Strain Name:

B6.FVB(Cg)-Mmp9tm1Tvu/J

Stock Number:

007084

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Because Mmp9tm1Tvu homozygous mice show altered inflammatory responses they may be used to study injury response and repair, angiogenesis and inflammatory response.

Description

Strain Information

Type Congenic; Targeted Mutation; Transgenic;
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Mating SystemHomozygote x Homozygote         (Female x Male)   04-JUN-09
Specieslaboratory mouse
GenerationN10F13 (06-AUG-14)
Generation Definitions
 
Donating Investigator IMR Colony,   The Jackson Laboratory

Description
Mice that are homozygous null for the Mmp9 (matrix metalloproteinase 9) gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to disrupt a most of exon 2 and all of intron 2 of the Mmp9 gene. The construct was electroporated into 129S-derived ZW4 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric male animals were mated with Swiss Black females. Progeny animals were mated to Black Swiss mice for an unknown number of generations before being mated with FVB/N animals. Upon arrival at The Jackson Laboratory mice, were mated to C57BL/6J animals for a minimum of N5 generations.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Mmp9tm1Tvu allele
004104   FVB.Cg-Mmp9tm1Tvu/J
View Strains carrying   Mmp9tm1Tvu     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Metaphyseal Anadysplasia 2; MANDP2   (MMP9)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Mmp9tm1Tvu/Mmp9tm1Tvu

        B6.129S6-Mmp9tm1Tvu
  • tumorigenesis
  • altered tumor morphology
    • injected A549 cells exhibit an increase in early apoptosis compared to in wild-type mice   (MGI Ref ID J:105098)
  • decreased tumor incidence
    • mice injected with Lewis lung carcinoma or A549 cells exhibit a decrease in tumors compared with similarly treated wild-type mice   (MGI Ref ID J:105098)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)
  • skeleton phenotype
  • abnormal long bone epiphyseal plate morphology
    • abnormal growth plate development, however after 3 weeks of age, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance except for the shorter long bones   (MGI Ref ID J:47297)
    • abnormal long bone hypertrophic chondrocyte zone
      • ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age   (MGI Ref ID J:47297)
      • apoptosis of hypertrophic chondrocytes is delayed   (MGI Ref ID J:47297)
      • by 3 weeks of age, when the hypertrophic zone is lengthened, aberrant apoptosis begins in the middle of the hypertrophic cartilage and is seen around the areas of ossification throughout the hypertrophic zone at 4 weeks   (MGI Ref ID J:47297)
      • increased width of hypertrophic chondrocyte zone
        • exhibit lengthened zone of hypertrophic cartilage with no difference in the reserve or proliferating zones   (MGI Ref ID J:47297)
  • abnormal metatarsal bone morphology
    • hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long   (MGI Ref ID J:47297)
  • abnormal trabecular bone morphology
    • area of metaphyseal trabecular bone is shorter   (MGI Ref ID J:47297)
  • decreased length of long bones
    • long bones are about 10% shorter than in wild-type   (MGI Ref ID J:47297)
    • short femur   (MGI Ref ID J:47297)
    • short tibia   (MGI Ref ID J:47297)
  • delayed bone ossification
    • secondary (epiphyseal) ossification sites are delayed until 2.5 weeks of age, however, by 3 weeks of age, these sites are completely ossified as in wild-type   (MGI Ref ID J:47297)
  • osteopetrosis
    • ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age and the ectopic ossification proceeds rapidly so that in some bones the entire zone of hypertrophic cartilage is ossified, leading to a large area of trabecular bone, however this is resolved with subsequent remodeling so that by 8 weeks, bones appear normal   (MGI Ref ID J:47297)
  • limbs/digits/tail phenotype
  • abnormal metatarsal bone morphology
    • hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long   (MGI Ref ID J:47297)
  • short femur   (MGI Ref ID J:47297)
  • short tibia   (MGI Ref ID J:47297)

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: FVB.129S6-Mmp9tm1Tvu or (involves: 129S6/SvEvTac)
  • cardiovascular system phenotype
  • altered response to myocardial infarction
    • exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type   (MGI Ref ID J:68211)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type   (MGI Ref ID J:68211)

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)
  • cardiovascular system phenotype
  • abnormal angiogenesis
    • exhibit reduced angiogenic response to peripheral leg ischemia; do not observe an increase in capillary density and see reduced capillary perfusion capacity and fewer points of capillary intersections (decreased branching) after ischemia   (MGI Ref ID J:95880)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac
  • mortality/aging
  • increased susceptibility to viral infection induced morbidity/mortality
    • CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • homeostasis/metabolism phenotype
  • abnormal chemokine level
    • ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
  • abnormal vascular wound healing
    • exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen   (MGI Ref ID J:109006)
  • decreased physiological sensitivity to xenobiotic
    • mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice   (MGI Ref ID J:84293)
    • mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
    • following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice   (MGI Ref ID J:84293)
    • ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
  • decreased susceptibility to injury
    • mice are resistant to the pathogenic activity of anti-mBP180 (Col17a1) antibodies that induce subepidermal blistering in wild-type mice   (MGI Ref ID J:91478)
    • however, mice reconstituted with wild-type neutrophils exhibit normal response to anti-Col17a1 antibodies   (MGI Ref ID J:91478)
    • mice are resistant to traumatic brain injury compared with similarly treated wild-type mice with smaller traumatic lesion volumes   (MGI Ref ID J:79422)
    • following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice   (MGI Ref ID J:62760)
    • however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms   (MGI Ref ID J:62760)
    • following IgG-induction of acute lung injury, mice exhibit reduced lung injury, decreased BALF protein leakage, and perivascular edema compared with similarly treated wild-type mice   (MGI Ref ID J:114188)
    • however, the number of macrophages and neutrophils recruited to the lungs is normal in mice with IgG-induced acute lung injury   (MGI Ref ID J:114188)
  • increased circulating interferon-beta level
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • increased circulating interferon-gamma level
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • immune system phenotype
  • abnormal chemokine level
    • ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
  • abnormal dendritic cell physiology
    • in vitro, chemotaxis of dendritic cells in response to CCL5 (RANTES) and CCL20 (MIP-3alpha) is impaired compared with similarly treated wild-type cells   (MGI Ref ID J:84293)
    • however, homing of dendritic cells from airways to lymph nodes in mice is normal   (MGI Ref ID J:84293)
    • abnormal Langerhans cell physiology
      • migration of Langerhans cells is impaired compared to in wild-type mice   (MGI Ref ID J:76157)
      • however, maturation of Langerhans cells is normal   (MGI Ref ID J:76157)
  • decreased IgE level
    • mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
  • decreased dendritic cell number
    • following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice   (MGI Ref ID J:84293)
  • decreased inflammatory response
    • mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice   (MGI Ref ID J:84293)
  • increased circulating interferon-beta level
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • increased circulating interferon-gamma level
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • increased susceptibility to viral infection
    • Coxsackievirus B3 (CVB3)-infected mice exhibit increased morbidity, viral load, serum IFN-gamma and IFN-beta, left ventricular posterior wall and interventricular septum thickness, and cardiac injury as determined by increased myocytolysis, calcification, and cellular infiltrate and decreased ejection fraction and E wave compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
    • increased susceptibility to viral infection induced morbidity/mortality
      • CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • myocarditis
    • CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • cardiovascular system phenotype
  • abnormal impulse conducting system conduction
    • on days 3 and 9, CVB3-infected mice exhibit decreased E wave compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • abnormal induced retinal neovascularization
    • mice exhibit 45% less ischemia-induced retinal neovascularization compared with similarly treated wild-type mice   (MGI Ref ID J:113620)
  • abnormal myocardial fiber physiology
    • myocytolysis is increased in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • abnormal vascular smooth muscle physiology
    • isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro   (MGI Ref ID J:109006)
  • abnormal vascular wound healing
    • exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen   (MGI Ref ID J:109006)
  • aortic aneurysm
    • following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice   (MGI Ref ID J:62760)
    • however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms   (MGI Ref ID J:62760)
  • cardiac fibrosis
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • decreased cardiac muscle contractility
    • on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • increased susceptibility to dystrophic cardiac calcinosis
    • in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • myocarditis
    • CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • thick interventricular septum
    • CVB3-infected mice exhibit increased interventricular septum thickness compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • thick ventricular wall
    • CVB3-infected mice exhibit increased left ventricular posterior wall thickness compared with similarly treated wild-type mice   (MGI Ref ID J:148442)
  • nervous system phenotype
  • abnormal myelination
    • exhibit decreased myelination in the corpus callosum at P7 and P10, but not at P14, as evidenced by decreased MBP expression   (MGI Ref ID J:105765)
  • decreased oligodendrocyte number
    • exhibit a decrease in the number of mature oligondendrocytes at P10, however no differences in oligodendrocyte precursor cell numbers   (MGI Ref ID J:105765)
  • muscle phenotype
  • abnormal vascular smooth muscle physiology
    • isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro   (MGI Ref ID J:109006)
  • decreased cardiac muscle contractility
    • on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice   (MGI Ref ID J:148442)
  • hematopoietic system phenotype
  • decreased IgE level
    • mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice   (MGI Ref ID J:84293)
  • decreased dendritic cell number
    • following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice   (MGI Ref ID J:84293)
  • vision/eye phenotype
  • abnormal induced retinal neovascularization
    • mice exhibit 45% less ischemia-induced retinal neovascularization compared with similarly treated wild-type mice   (MGI Ref ID J:113620)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * C57BL/6J
  • cardiovascular system phenotype
  • abnormal angiogenesis
    • exhibit significantly reduced carotid artery intimal hyperplasia in response to vascular injury and fewer intimal smooth muscle cells   (MGI Ref ID J:101783)
  • abnormal vascular smooth muscle physiology
    • exhibit impairment of smooth muscle cell migration through a gelatin-coated membrane towards a chemoattractant and in a wound assay4   (MGI Ref ID J:101783)
    • isolated smooth muscle cells exhibit impaired ability to compact collagen gels, to assemble fibrillar collagen from exogenous monomers, and to attach to gelatin   (MGI Ref ID J:101783)
  • muscle phenotype
  • abnormal vascular smooth muscle physiology
    • exhibit impairment of smooth muscle cell migration through a gelatin-coated membrane towards a chemoattractant and in a wound assay4   (MGI Ref ID J:101783)
    • isolated smooth muscle cells exhibit impaired ability to compact collagen gels, to assemble fibrillar collagen from exogenous monomers, and to attach to gelatin   (MGI Ref ID J:101783)

Mmp9tm1Tvu/Mmp9tm1Tvu

        FVB.129S6-Mmp9tm1Tvu
  • mortality/aging
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice   (MGI Ref ID J:104644)
    • however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis   (MGI Ref ID J:104644)
  • cardiovascular system phenotype
  • abnormal physiological neovascularization
    • exhibit increased neovascularization post myocardial infarction, as shown by increased total vessel density and normalized vessel distribution between subendo- and epicardial regions relative to wild-type after coronary artery ligation   (MGI Ref ID J:104786)
  • altered response to myocardial infarction
    • exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction   (MGI Ref ID J:104786)
  • increased angiogenesis
    • exhibit an increased angiogenic potential after myocardial infarction, as shown by the presence of newly formed vessels in the infarct region   (MGI Ref ID J:104786)
  • increased ventricle muscle contractility
    • exhibit higher end-systolic pressure and dP/dtmax than wild-type after myocardial infarction, despite similar infarct sizes   (MGI Ref ID J:104786)
  • immune system phenotype
  • *normal* immune system phenotype   (MGI Ref ID J:104644)
    • abnormal neutrophil physiology
      • neutrophil chemotatic response to fMLP is greater than for wild-type cells   (MGI Ref ID J:104644)
      • polymononuclear cell migration through Matri-gel-coated membrane in response to fMLP is greater compared with similarly treated wild-type cells   (MGI Ref ID J:104644)
    • decreased susceptibility to induced colitis
      • DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type mice   (MGI Ref ID J:104644)
      • mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice   (MGI Ref ID J:104644)
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction
    • exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction   (MGI Ref ID J:104786)
  • decreased sensitivity to xenobiotic induced morbidity/mortality
    • DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice   (MGI Ref ID J:104644)
    • however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis   (MGI Ref ID J:104644)
  • muscle phenotype
  • increased ventricle muscle contractility
    • exhibit higher end-systolic pressure and dP/dtmax than wild-type after myocardial infarction, despite similar infarct sizes   (MGI Ref ID J:104786)
  • digestive/alimentary phenotype
  • decreased susceptibility to induced colitis
    • DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type mice   (MGI Ref ID J:104644)
    • mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice   (MGI Ref ID J:104644)
  • hematopoietic system phenotype
  • abnormal neutrophil physiology
    • neutrophil chemotatic response to fMLP is greater than for wild-type cells   (MGI Ref ID J:104644)
    • polymononuclear cell migration through Matri-gel-coated membrane in response to fMLP is greater compared with similarly treated wild-type cells   (MGI Ref ID J:104644)

Mmp9tm1Tvu/Mmp9tm1Tvu

        129S6/SvEvTac-Mmp9tm1Tvu
  • immune system phenotype
  • *normal* immune system phenotype
    • mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis   (MGI Ref ID J:113463)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129/Sv * 129S6/SvEvTac
  • homeostasis/metabolism phenotype
  • decreased circulating interleukin-10 level
    • DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure   (MGI Ref ID J:55723)
  • immune system phenotype
  • decreased circulating interleukin-10 level
    • DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure   (MGI Ref ID J:55723)
  • increased susceptibility to type IV hypersensitivity reaction
    • DNFB-sensitized and challenged mice exhibit a prolonged response and delayed resolution of inflammation compared with similarly treated wild-type mice   (MGI Ref ID J:55723)
    • however, resolution of phenol elicited inflammation is normal   (MGI Ref ID J:55723)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * CD-1
  • mortality/aging
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • following myelodepletion with 5-fluorouracil (5-FU), 72% of mice die unlike similarly treated wild-type mice   (MGI Ref ID J:149957)
  • hematopoietic system phenotype
  • abnormal bone marrow cell physiology
    • in transplantation experiments, chemokine-induced mobilization of bone marrow repopulating cells is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
    • mobilization of bone-marrow derived circulating endothelial cell progenitors is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • abnormal hematopoietic stem cell morphology
    • following myelodepletion with 5-fluorouracil (5-FU), fewer hematopoietic stem cells enter S phase compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • abnormal megakaryocyte differentiation
    • restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • impaired hematopoiesis
    • following myelodepletion with 5-fluorouracil (5-FU), mice exhibit delayed recovery compared with similarly treated wild-type mice   (MGI Ref ID J:149957)
  • impaired myelopoiesis
    • restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • homeostasis/metabolism phenotype
  • decreased susceptibility to injury
    • following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice   (MGI Ref ID J:129161)
    • decreased susceptibility to ischemic brain injury
      • 24 hours following cerebral ischemia, mice exhibit reduced ischemic lesion volumes compared with similarly treated wild-type mice   (MGI Ref ID J:79535)
      • however, mice subjected to cerebral ischemia exhibit normal neurological deficits   (MGI Ref ID J:79535)
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • following myelodepletion with 5-fluorouracil (5-FU), 72% of mice die unlike similarly treated wild-type mice   (MGI Ref ID J:149957)
  • nervous system phenotype
  • decreased susceptibility to ischemic brain injury
    • 24 hours following cerebral ischemia, mice exhibit reduced ischemic lesion volumes compared with similarly treated wild-type mice   (MGI Ref ID J:79535)
    • however, mice subjected to cerebral ischemia exhibit normal neurological deficits   (MGI Ref ID J:79535)
  • immune system phenotype
  • impaired myelopoiesis
    • restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • vision/eye phenotype
  • abnormal retinal apoptosis
    • following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice   (MGI Ref ID J:129161)
  • cellular phenotype
  • abnormal megakaryocyte differentiation
    • restoration of myeloid and megakaryotic lineages in 5-FU-treated mice is impaired compared to in similarly treated wild-type mice   (MGI Ref ID J:149957)
  • abnormal retinal apoptosis
    • following optic nerve ligation, retinas fail to exhibit apoptosis unlike in similarly treated wild-type mice   (MGI Ref ID J:129161)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * C57BL/6
  • immune system phenotype
  • abnormal chemokine level
    • on day 24, alum treated mice exhibit an increase in CCL22 in lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on days 24 and 30, ovalbumin-treated mice exhibit increased CCL11 in the bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on day 24, ovalbumin-treated mice exhibit an increase in bronchoalveolar lavage CCL22 compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on day 30, ovalbumin-treated mice exhibit an increase in lung tissue CCL22 compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • however, mice exhibit normal levels of CCL2, CCL3, and CCL5 following ovalbumin treatment   (MGI Ref ID J:88065)
  • abnormal cytokine secretion   (MGI Ref ID J:88065)
    • decreased interferon-gamma secretion
      • ovalbumin-treated mice exhibit decreased IFN-gamma in bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased interferon-gamma secretion
      • on day 24, T cells from alum-treated mice exhibit increased IFN-gamma secretion compared with cells from similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased interleukin-13 secretion
      • ovalbumin-treated mice exhibit increased IL13 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased interleukin-4 secretion
      • ovalbumin-treated mice exhibit increased IL4 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
      • on day 24, T cells from ovalbumin-treated mice exhibit increased IL4 secretion compared with cells from similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased interleukin-5 secretion
      • ovalbumin-treated mice exhibit increased IL5 in lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • abnormal leukocyte morphology   (MGI Ref ID J:88065)
    • increased T cell proliferation
      • on day 24 hours in ovalbumin-treated wild-type mice compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased eosinophil cell number
      • on days 24 and 30, ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue eosinophil numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased lymphocyte cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue lymphocyte numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
      • increased T-helper 2 cell number
        • on day 24, ovalbumin-treated mice exhibit an increased in Th2 helper cells in the bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased macrophage cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue macrophage cell numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased monocyte cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue monocyte numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • abnormal response to infection
    • mice infected with Streptoccocus pneumoniae to in the right forebrain exhibit higher blood and spleen bacterial titers compared with similarly treated wild-type mice   (MGI Ref ID J:126519)
    • in experimental peritonitis, mice exhibit higher spleen bacterial titers compared with similarly treated wild-type mice   (MGI Ref ID J:126519)
  • increased IgE level
    • ovalbumin-treated mice exhibit increased ovalbumin-IgE compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • lung inflammation
    • ovalbumin-treated mice exhibit increased lung inflammation with increased total cells, eosinophils, macrophages, lymphocytes, and monocytes in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • homeostasis/metabolism phenotype
  • abnormal chemokine level
    • on day 24, alum treated mice exhibit an increase in CCL22 in lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on days 24 and 30, ovalbumin-treated mice exhibit increased CCL11 in the bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on day 24, ovalbumin-treated mice exhibit an increase in bronchoalveolar lavage CCL22 compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • on day 30, ovalbumin-treated mice exhibit an increase in lung tissue CCL22 compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • however, mice exhibit normal levels of CCL2, CCL3, and CCL5 following ovalbumin treatment   (MGI Ref ID J:88065)
  • respiratory system phenotype
  • lung inflammation
    • ovalbumin-treated mice exhibit increased lung inflammation with increased total cells, eosinophils, macrophages, lymphocytes, and monocytes in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • hematopoietic system phenotype
  • abnormal leukocyte morphology   (MGI Ref ID J:88065)
    • increased T cell proliferation
      • on day 24 hours in ovalbumin-treated wild-type mice compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased eosinophil cell number
      • on days 24 and 30, ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue eosinophil numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased lymphocyte cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue lymphocyte numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
      • increased T-helper 2 cell number
        • on day 24, ovalbumin-treated mice exhibit an increased in Th2 helper cells in the bronchoalveolar lavage compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased macrophage cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue macrophage cell numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
    • increased monocyte cell number
      • ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue monocyte numbers compared with similarly treated wild-type mice   (MGI Ref ID J:88065)
  • increased IgE level
    • ovalbumin-treated mice exhibit increased ovalbumin-IgE compared with similarly treated wild-type mice   (MGI Ref ID J:88065)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * FVB/N
  • nervous system phenotype
  • decreased neuron apoptosis
    • wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells   (MGI Ref ID J:96548)
  • homeostasis/metabolism phenotype
  • delayed wound healing
    • at days 3, 5, and 7, mice exhibit delayed wound compared with similarly treated wild-type mice   (MGI Ref ID J:150790)
  • cellular phenotype
  • decreased neuron apoptosis
    • wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells   (MGI Ref ID J:96548)

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac
  • behavior/neurological phenotype
  • impaired contextual conditioning behavior
    • when tested at 24 hours, mice exhibit reduced memory in hippocampus-dependent context conditioning compared with similarly treated wild-type mice   (MGI Ref ID J:105763)
    • however, mice tested at 30 hours for cued conditioning is normal   (MGI Ref ID J:105763)
  • nervous system phenotype
  • reduced long term potentiation
    • long term potentiation is smaller in magnitude and shorter in duration than in wild-type mice   (MGI Ref ID J:105763)
    • however, mice exhibit normal NMDA receptor-dependent long term depression and paired pulse facilitation   (MGI Ref ID J:105763)

Mmp9tm1Tvu/Mmp9tm1Tvu

        FVB.Cg-Mmp9tm1Tvu/J
  • mortality/aging
  • decreased susceptibility to viral infection induced morbidity/mortality
    • mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice   (MGI Ref ID J:153406)
    • however, mice exhibit a normal survival when injected intracerebrally with West Nile virus   (MGI Ref ID J:153406)
  • immune system phenotype
  • decreased susceptibility to viral infection
    • mice infected with West Nile virus exhibit decreased mortality, brain viral load, CD45+ leukocyte infiltration into brain tissue, and blood brain barrier permeability compared with similarly treated wild-type mice   (MGI Ref ID J:153406)
    • however, mice exhibit a normal response to West Nile virus infection when injected intracerebrally with the virus   (MGI Ref ID J:153406)
    • decreased susceptibility to viral infection induced morbidity/mortality
      • mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice   (MGI Ref ID J:153406)
      • however, mice exhibit a normal survival when injected intracerebrally with West Nile virus   (MGI Ref ID J:153406)
  • digestive/alimentary phenotype
  • abnormal intestinal goblet cell morphology
    • mice exhibit an increased in the number of intestinal goblet cells compared to in wild-type mice   (MGI Ref ID J:128322)
    • however, the number of goblet cells per crypt is normal   (MGI Ref ID J:128322)
  • behavior/neurological phenotype
  • hypoalgesia
    • 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice   (MGI Ref ID J:133660)
    • however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation   (MGI Ref ID J:133660)
  • homeostasis/metabolism phenotype
  • abnormal response/metabolism to endogenous compounds
    • mice treated with tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12) exhibit increased body and muscle weight, intact basement membrane, and reduced myopathy, clustering of inflammatory cells, and number of necrotic fibers in the muscle compared with similarly treated wild-type mice   (MGI Ref ID J:147593)
  • decreased susceptibility to injury
    • 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice   (MGI Ref ID J:133660)
    • however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation   (MGI Ref ID J:133660)
    • following hepatic ischemia and reperfusion, hepatic apoptosis is decreased compared to in similarly treated wild-type mice   (MGI Ref ID J:148923)
  • cardiovascular system phenotype
  • abnormal blood-brain barrier function
    • mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice   (MGI Ref ID J:153406)
  • nervous system phenotype
  • abnormal blood-brain barrier function
    • mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice   (MGI Ref ID J:153406)
  • growth/size/body phenotype
  • increased body weight
    • in tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12)-treated mice compared with similarly treated wild-type mice   (MGI Ref ID J:147593)
  • muscle phenotype
  • increased tibialis anterior weight
    • the weight of the tibialis anterior in mice treated with Tnfsf12-treated mice is greater than in similarly treated wild-type mice   (MGI Ref ID J:147593)
  • integument phenotype
  • hypoalgesia
    • 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice   (MGI Ref ID J:133660)
    • however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation   (MGI Ref ID J:133660)

Mmp9tm1Tvu/Mmp9tm1Tvu

        C3N.129S6-Mmp9tm1Tvu
  • immune system phenotype
  • decreased susceptibility to bacterial infection
    • mice infected with Borrelia burgdorferi exhibit less ankle swelling, joint inflammation, and arthritis than similarly treated wild-type mice   (MGI Ref ID J:150311)
    • however, mice exhibit normal development of carditis when infected with B. burgdorferi   (MGI Ref ID J:150311)
  • joint inflammation
    • in B. burgdorferi-infected mice compared with similarly treated wild-type mice   (MGI Ref ID J:150311)
    • decreased susceptibility to induced arthritis
      • B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice   (MGI Ref ID J:150311)
      • however, spirochete numbers in the joint are normal   (MGI Ref ID J:150311)
  • skeleton phenotype
  • joint inflammation
    • in B. burgdorferi-infected mice compared with similarly treated wild-type mice   (MGI Ref ID J:150311)
    • decreased susceptibility to induced arthritis
      • B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice   (MGI Ref ID J:150311)
      • however, spirochete numbers in the joint are normal   (MGI Ref ID J:150311)
  • joint swelling
    • in B. burgdorferi-infected mice compared with similarly treated wild-type mice   (MGI Ref ID J:150311)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Cardiovascular Research
Ischemia studies

Developmental Biology Research
Defects in Extracellular Matrix Molecules
Skeletal Defects

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology, Inflammation and Autoimmunity Research
Inflammation

Internal/Organ Research
Skeleton

Sensorineural Research
Nociception

Mmp9tm1Tvu related

Cancer Research
Increased Tumor Incidence
      Skin Cancers
      Skin Cancers: Resistant

Developmental Biology Research
Defects in Extracellular Matrix Molecules

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology, Inflammation and Autoimmunity Research
Inflammation

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Mmp9tm1Tvu
Allele Name targeted mutation 1, Thiennu H Vu
Allele Type Targeted (Null/Knockout)
Common Name(s) GelB-; Gelatinase B-Null; MMP-9 KO; MMP-9-; MMP-9KO; MMP9-; Mmp9-;
Mutation Made By Zena Werb,   University of California, San Francisco
Strain of Origin129S6/SvEvTac
ES Cell Line NameOther (see notes)
ES Cell Line Strain129
Gene Symbol and Name Mmp9, matrix metallopeptidase 9
Chromosome 2
Gene Common Name(s) AW743869; B/MMP9; CLG4B; Clg4b; GELB; Gel B; Gelatinase B; MANDP2; MMP-9; collagenase IVB, basement membrane, 92 kDa; expressed sequence AW743869;
General Note ES cell line = ZW4.
Molecular Note Part of exon 2 and all of intron 2 were replaced with a cassette containing the neomycin resistance gene driven by a PGK promoter. [MGI Ref ID J:47297]

Genotyping

Genotyping Information

Genotyping Protocols

Mmp9tm1Tvu, Melt Curve Analysis
Mmp9 tm1Tvu, Standard PCR
Mmp9tm1Tvu, Fast MCA


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Coussens LM; Tinkle CL; Hanahan D; Werb Z. 2000. MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis Cell 103(3):481-90. [PubMed: 11081634]  [MGI Ref ID J:65699]

Additional References

Mmp9tm1Tvu related

Acuff HB; Carter KJ; Fingleton B; Gorden DL; Matrisian LM. 2006. Matrix metalloproteinase-9 from bone marrow-derived cells contributes to survival but not growth of tumor cells in the lung microenvironment. Cancer Res 66(1):259-66. [PubMed: 16397239]  [MGI Ref ID J:105098]

Ahn GO; Brown JM. 2008. Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cells. Cancer Cell 13(3):193-205. [PubMed: 18328424]  [MGI Ref ID J:132946]

Allport JR; Lim YC; Shipley JM; Senior RM; Shapiro SD; Matsuyoshi N; Vestweber D; Luscinskas FW. 2002. Neutrophils from MMP-9- or neutrophil elastase-deficient mice show no defect in transendothelial migration under flow in vitro. J Leukoc Biol 71(5):821-8. [PubMed: 11994507]  [MGI Ref ID J:76606]

Alvarez JI; Teale JM. 2007. Evidence for differential changes of junctional complex proteins in murine neurocysticercosis dependent upon CNS vasculature. Brain Res 1169:98-111. [PubMed: 17686468]  [MGI Ref ID J:145255]

Andrews KL; Betsuyaku T; Rogers S; Shipley JM; Senior RM; Miner JH. 2000. Gelatinase B (MMP-9) is not essential in the normal kidney and does not influence progression of renal disease in a mouse model of alport syndrome Am J Pathol 157(1):303-11. [PubMed: 10880400]  [MGI Ref ID J:63137]

Arnould C; Lelievre-Pegorier M; Ronco P; Lelongt B. 2009. MMP9 limits apoptosis and stimulates branching morphogenesis during kidney development. J Am Soc Nephrol 20(10):2171-80. [PubMed: 19713309]  [MGI Ref ID J:166319]

Asahi M; Asahi K; Jung JC; del Zoppo GJ; Fini ME; Lo EH. 2000. Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94. J Cereb Blood Flow Metab 20(12):1681-9. [PubMed: 11129784]  [MGI Ref ID J:79535]

Asahi M; Wang X; Mori T; Sumii T; Jung JC; Moskowitz MA; Fini ME; Lo EH. 2001. Effects of matrix metalloproteinase-9 gene knock-out on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia. J Neurosci 21(19):7724-32. [PubMed: 11567062]  [MGI Ref ID J:71686]

Awla D; Abdulla A; Syk I; Jeppsson B; Regner S; Thorlacius H. 2012. Neutrophil-derived matrix metalloproteinase-9 is a potent activator of trypsinogen in acinar cells in acute pancreatitis. J Leukoc Biol 91(5):711-9. [PubMed: 22100390]  [MGI Ref ID J:183726]

Bajor M; Michaluk P; Gulyassy P; Kekesi AK; Juhasz G; Kaczmarek L. 2012. Synaptic cell adhesion molecule-2 and collapsin response mediator protein-2 are novel members of the matrix metalloproteinase-9 degradome. J Neurochem 122(4):775-88. [PubMed: 22694054]  [MGI Ref ID J:187509]

Baluk P; Raymond WW; Ator E; Coussens LM; McDonald DM; Caughey GH. 2004. Matrix metalloproteinase-2 and -9 expression increases in Mycoplasma-infected airways but is not required for microvascular remodeling. Am J Physiol Lung Cell Mol Physiol 287(2):L307-17. [PubMed: 15075248]  [MGI Ref ID J:108152]

Barnett JM; McCollum GW; Fowler JA; Duan JJ; Kay JD; Liu RQ; Bingaman DP; Penn JS. 2007. Pharmacologic and genetic manipulation of MMP-2 and -9 affects retinal neovascularization in rodent models of OIR. Invest Ophthalmol Vis Sci 48(2):907-15. [PubMed: 17251494]  [MGI Ref ID J:123262]

Bengatta S; Arnould C; Letavernier E; Monge M; de Preneuf HM; Werb Z; Ronco P; Lelongt B. 2009. MMP9 and SCF protect from apoptosis in acute kidney injury. J Am Soc Nephrol 20(4):787-97. [PubMed: 19329763]  [MGI Ref ID J:164043]

Benson HL; Mobashery S; Chang M; Kheradmand F; Hong JS; Smith GN; Shilling RA; Wilkes DS. 2011. Endogenous matrix metalloproteinases 2 and 9 regulate activation of CD4+ and CD8+ T cells. Am J Respir Cell Mol Biol 44(5):700-8. [PubMed: 20639459]  [MGI Ref ID J:185032]

Bergers G; Brekken R; McMahon G; Vu TH; Itoh T; Tamaki K; Tanzawa K; Thorpe P; Itohara S; Werb Z; Hanahan D. 2000. Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis Nat Cell Biol 2(10):737-44. [PubMed: 11025665]  [MGI Ref ID J:65019]

Betsuyaku T; Fukuda Y; Parks WC; Shipley JM; Senior RM. 2000. Gelatinase B is required for alveolar bronchiolization after intratracheal bleomycin. Am J Pathol 157(2):525-35. [PubMed: 10934155]  [MGI Ref ID J:108171]

Bonig H; Priestley GV; Oehler V; Papayannopoulou T. 2007. Hematopoietic progenitor cells (HPC) from mobilized peripheral blood display enhanced migration and marrow homing compared to steady-state bone marrow HPC. Exp Hematol 35(2):326-34. [PubMed: 17258081]  [MGI Ref ID J:123189]

Bottcher T; Spreer A; Azeh I; Nau R; Gerber J. 2003. Matrix metalloproteinase-9 deficiency impairs host defense mechanisms against Streptococcus pneumoniae in a mouse model of bacterial meningitis. Neurosci Lett 338(3):201-4. [PubMed: 12581831]  [MGI Ref ID J:126519]

Bradley LM; Douglass MF; Chatterjee D; Akira S; Baaten BJ. 2012. Matrix metalloprotease 9 mediates neutrophil migration into the airways in response to influenza virus-induced toll-like receptor signaling. PLoS Pathog 8(4):e1002641. [PubMed: 22496659]  [MGI Ref ID J:195392]

Brass DM; Hollingsworth JW; Cinque M; Li Z; Potts E; Toloza E; Foster WM; Schwartz DA. 2008. Chronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosis. Am J Respir Cell Mol Biol 39(5):584-90. [PubMed: 18539952]  [MGI Ref ID J:154269]

Bruni-Cardoso A; Johnson LC; Vessella RL; Peterson TE; Lynch CC. 2010. Osteoclast-derived matrix metalloproteinase-9 directly affects angiogenesis in the prostate tumor-bone microenvironment. Mol Cancer Res 8(4):459-70. [PubMed: 20332212]  [MGI Ref ID J:205237]

Budatha M; Roshanravan S; Zheng Q; Weislander C; Chapman SL; Davis EC; Starcher B; Word RA; Yanagisawa H. 2011. Extracellular matrix proteases contribute to progression of pelvic organ prolapse in mice and humans. J Clin Invest 121(5):2048-59. [PubMed: 21519142]  [MGI Ref ID J:173933]

Cackowski FC; Anderson JL; Patrene KD; Choksi RJ; Shapiro SD; Windle JJ; Blair HC; Roodman GD. 2010. Osteoclasts are important for bone angiogenesis. Blood 115(1):140-9. [PubMed: 19887675]  [MGI Ref ID J:156315]

Camp TM; Tyagi SC; Senior RM; Hayden MR; Tyagi SC. 2003. Gelatinase B(MMP-9) an apoptotic factor in diabetic transgenic mice. Diabetologia 46(10):1438-45. [PubMed: 12928773]  [MGI Ref ID J:86293]

Carmeliet P; Moons L; Lijnen R; Baes M; Lemaitre V; Tipping P; Drew A; Eeckhout Y; Shapiro S; Lupu F; Collen D. 1997. Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation. Nat Genet 17(4):439-44. [PubMed: 9398846]  [MGI Ref ID J:44387]

Castaneda FE; Walia B; Vijay-Kumar M; Patel NR; Roser S; Kolachala VL; Rojas M; Wang L; Oprea G; Garg P; Gewirtz AT; Roman J; Merlin D; Sitaraman SV. 2005. Targeted deletion of metalloproteinase 9 attenuates experimental colitis in mice: central role of epithelial-derived MMP. Gastroenterology 129(6):1991-2008. [PubMed: 16344067]  [MGI Ref ID J:104644]

Cataldo DD; Tournoy KG; Vermaelen K; Munaut C; Foidart JM; Louis R; Noel A; Pauwels RA. 2002. Matrix metalloproteinase-9 deficiency impairs cellular infiltration and bronchial hyperresponsiveness during allergen-induced airway inflammation. Am J Pathol 161(2):491-8. [PubMed: 12163374]  [MGI Ref ID J:113541]

Chattopadhyay S; Shubayev VI. 2009. MMP-9 controls Schwann cell proliferation and phenotypic remodeling via IGF-1 and ErbB receptor-mediated activation of MEK/ERK pathway. Glia 57(12):1316-25. [PubMed: 19229995]  [MGI Ref ID J:156203]

Chetty A; Cao GJ; Severgnini M; Simon A; Warburton R; Nielsen HC. 2008. Role of matrix metalloprotease-9 in hyperoxic injury in developing lung. Am J Physiol Lung Cell Mol Physiol 295(4):L584-92. [PubMed: 18658276]  [MGI Ref ID J:141981]

Cheung C; Marchant D; Walker EK; Luo Z; Zhang J; Yanagawa B; Rahmani M; Cox J; Overall C; Senior RM; Luo H; McManus BM. 2008. Ablation of matrix metalloproteinase-9 increases severity of viral myocarditis in mice. Circulation 117(12):1574-82. [PubMed: 18332263]  [MGI Ref ID J:148442]

Chiao YA; Ramirez TA; Zamilpa R; Okoronkwo SM; Dai Q; Zhang J; Jin YF; Lindsey ML. 2012. Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice. Cardiovasc Res 96(3):444-55. [PubMed: 22918978]  [MGI Ref ID J:210077]

Chintala SK; Zhang X; Austin JS; Fini ME. 2002. Deficiency in matrix metalloproteinase gelatinase B (MMP-9) protects against retinal ganglion cell death after optic nerve ligation. J Biol Chem 277(49):47461-8. [PubMed: 12354772]  [MGI Ref ID J:129161]

Cho A; Reidy MA. 2002. Matrix metalloproteinase-9 is necessary for the regulation of smooth muscle cell replication and migration after arterial injury. Circ Res 91(9):845-51. [PubMed: 12411400]  [MGI Ref ID J:109007]

Choi ET; Collins ET; Marine LA; Uberti MG; Uchida H; Leidenfrost JE; Khan MF; Boc KP; Abendschein DR; Parks WC. 2005. Matrix metalloproteinase-9 modulation by resident arterial cells is responsible for injury-induced accelerated atherosclerotic plaque development in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 25(5):1020-5. [PubMed: 15746435]  [MGI Ref ID J:110044]

Chun TH; Hotary KB; Sabeh F; Saltiel AR; Allen ED; Weiss SJ. 2006. A pericellular collagenase directs the 3-dimensional development of white adipose tissue. Cell 125(3):577-91. [PubMed: 16678100]  [MGI Ref ID J:115867]

Chun TH; Sabeh F; Ota I; Murphy H; McDonagh KT; Holmbeck K; Birkedal-Hansen H; Allen ED; Weiss SJ. 2004. MT1-MMP-dependent neovessel formation within the confines of the three-dimensional extracellular matrix. J Cell Biol 167(4):757-67. [PubMed: 15545316]  [MGI Ref ID J:94371]

Colnot C; Thompson Z; Miclau T; Werb Z; Helms JA. 2003. Altered fracture repair in the absence of MMP9. Development 130(17):4123-33. [PubMed: 12874132]  [MGI Ref ID J:91527]

Copin JC; Bengualid DJ; Da Silva RF; Kargiotis O; Schaller K; Gasche Y. 2011. Recombinant tissue plasminogen activator induces blood-brain barrier breakdown by a matrix metalloproteinase-9-independent pathway after transient focal cerebral ischemia in mouse. Eur J Neurosci 34(7):1085-92. [PubMed: 21895804]  [MGI Ref ID J:178013]

Copin JC; Gasche Y. 2007. Matrix metalloproteinase-9 deficiency has no effect on glial scar formation after transient focal cerebral ischemia in mouse. Brain Res 1150:167-73. [PubMed: 17434457]  [MGI Ref ID J:122495]

Corry DB; Kiss A; Song LZ; Song L; Xu J; Lee SH; Werb Z; Kheradmand F. 2004. Overlapping and independent contributions of MMP2 and MMP9 to lung allergic inflammatory cell egression through decreased CC chemokines. FASEB J 18(9):995-7. [PubMed: 15059974]  [MGI Ref ID J:118113]

Costanzo RM; Perrino LA. 2008. Peak in matrix metaloproteinases-2 levels observed during recovery from olfactory nerve injury. Neuroreport 19(3):327-31. [PubMed: 18303576]  [MGI Ref ID J:133918]

Dahiya S; Bhatnagar S; Hindi SM; Jiang C; Paul PK; Kuang S; Kumar A. 2011. Elevated levels of active matrix metalloproteinase-9 cause hypertrophy in skeletal muscle of normal and dystrophin-deficient mdx mice. Hum Mol Genet 20(22):4345-59. [PubMed: 21846793]  [MGI Ref ID J:176891]

Dahiya S; Givvimani S; Bhatnagar S; Qipshidze N; Tyagi SC; Kumar A. 2011. Osteopontin-stimulated expression of matrix metalloproteinase-9 causes cardiomyopathy in the mdx model of Duchenne muscular dystrophy. J Immunol 187(5):2723-31. [PubMed: 21810612]  [MGI Ref ID J:179125]

Deshmukh HS; Shaver C; Case LM; Dietsch M; Wesselkamper SC; Hardie WD; Korfhagen TR; Corradi M; Nadel JA; Borchers MT; Leikauf GD. 2008. Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin production. Am J Respir Cell Mol Biol 38(4):446-54. [PubMed: 18006877]  [MGI Ref ID J:149725]

Du R; Lu KV; Petritsch C; Liu P; Ganss R; Passegue E; Song H; Vandenberg S; Johnson RS; Werb Z; Bergers G. 2008. HIF1alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion. Cancer Cell 13(3):206-20. [PubMed: 18328425]  [MGI Ref ID J:132945]

Ducharme A; Frantz S; Aikawa M; Rabkin E; Lindsey M; Rohde LE; Schoen FJ; Kelly RA; Werb Z; Libby P; Lee RT. 2000. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest 106(1):55-62. [PubMed: 10880048]  [MGI Ref ID J:68211]

Filippov S; Koenig GC; Chun TH; Hotary KB; Ota I; Bugge TH; Roberts JD; Fay WP; Birkedal-Hansen H; Holmbeck K; Sabeh F; Allen ED; Weiss SJ. 2005. MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells. J Exp Med 202(5):663-71. [PubMed: 16147977]  [MGI Ref ID J:100717]

Fleetwood AJ; Achuthan A; Schultz H; Nansen A; Almholt K; Usher P; Hamilton JA. 2014. Urokinase plasminogen activator is a central regulator of macrophage three-dimensional invasion, matrix degradation, and adhesion. J Immunol 192(8):3540-7. [PubMed: 24616477]  [MGI Ref ID J:210232]

Galis ZS; Johnson C; Godin D; Magid R; Shipley JM; Senior RM; Ivan E. 2002. Targeted disruption of the matrix metalloproteinase-9 gene impairs smooth muscle cell migration and geometrical arterial remodeling. Circ Res 91(9):852-9. [PubMed: 12411401]  [MGI Ref ID J:109006]

Garg P; Ravi A; Patel NR; Roman J; Gewirtz AT; Merlin D; Sitaraman SV. 2007. Matrix metalloproteinase-9 regulates MUC-2 expression through its effect on goblet cell differentiation. Gastroenterology 132(5):1877-89. [PubMed: 17484881]  [MGI Ref ID J:128322]

Garg P; Sarma D; Jeppsson S; Patel NR; Gewirtz AT; Merlin D; Sitaraman SV. 2010. Matrix metalloproteinase-9 functions as a tumor suppressor in colitis-associated cancer. Cancer Res 70(2):792-801. [PubMed: 20068187]  [MGI Ref ID J:156749]

Gidday JM; Gasche YG; Copin JC; Shah AR; Perez RS; Shapiro SD; Chan PH; Park TS. 2005. Leukocyte-derived matrix metalloproteinase-9 mediates blood-brain barrier breakdown and is proinflammatory after transient focal cerebral ischemia. Am J Physiol Heart Circ Physiol 289(2):H558-68. [PubMed: 15764676]  [MGI Ref ID J:100320]

Gieling RG; Wallace K; Han YP. 2009. Interleukin-1 participates in the progression from liver injury to fibrosis. Am J Physiol Gastrointest Liver Physiol 296(6):G1324-31. [PubMed: 19342509]  [MGI Ref ID J:149597]

Giraudo E; Inoue M; Hanahan D. 2004. An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis. J Clin Invest 114(5):623-33. [PubMed: 15343380]  [MGI Ref ID J:92599]

Givvimani S; Munjal C; Narayanan N; Aqil F; Tyagi G; Metreveli N; Tyagi SC. 2012. Hyperhomocysteinemia decreases intestinal motility leading to constipation. Am J Physiol Gastrointest Liver Physiol 303(3):G281-90. [PubMed: 22595990]  [MGI Ref ID J:191361]

Gong Y; Hart E; Shchurin A; Hoover-Plow J. 2008. Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice. J Clin Invest 118(9):3012-24. [PubMed: 18677407]  [MGI Ref ID J:140977]

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Kenny HA; Kaur S; Coussens LM; Lengyel E. 2008. The initial steps of ovarian cancer cell metastasis are mediated by MMP-2 cleavage of vitronectin and fibronectin. J Clin Invest 118(4):1367-79. [PubMed: 18340378]  [MGI Ref ID J:135977]

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Korol A; Pino G; Dwivedi D; Robertson JV; Deschamps PA; West-Mays JA. 2014. Matrix Metalloproteinase-9-Null Mice Are Resistant to TGF-beta-Induced Anterior Subcapsular Cataract Formation. Am J Pathol 184(7):2001-12. [PubMed: 24814605]  [MGI Ref ID J:211036]

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Lian X; Qin Y; Hossain SA; Yang L; White A; Xu H; Shipley JM; Li T; Senior RM; Du H; Yan C. 2005. Overexpression of Stat3C in pulmonary epithelium protects against hyperoxic lung injury. J Immunol 174(11):7250-6. [PubMed: 15905571]  [MGI Ref ID J:98964]

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Lin CH; Lee HT; Lee SD; Lee W; Cho CW; Lin SZ; Wang HJ; Okano H; Su CY; Yu YL; Hsu CY; Shyu WC. 2013. Role of HIF-1alpha-activated Epac1 on HSC-mediated neuroplasticity in stroke model. Neurobiol Dis 58:76-91. [PubMed: 23702312]  [MGI Ref ID J:201546]

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Littlepage LE; Sternlicht MD; Rougier N; Phillips J; Gallo E; Yu Y; Williams K; Brenot A; Gordon JI; Werb Z. 2010. Matrix metalloproteinases contribute distinct roles in neuroendocrine prostate carcinogenesis, metastasis, and angiogenesis progression. Cancer Res 70(6):2224-34. [PubMed: 20215503]  [MGI Ref ID J:157977]

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Martin MD; Carter KJ; Jean-Philippe SR; Chang M; Mobashery S; Thiolloy S; Lynch CC; Matrisian LM; Fingleton B. 2008. Effect of ablation or inhibition of stromal matrix metalloproteinase-9 on lung metastasis in a breast cancer model is dependent on genetic background. Cancer Res 68(15):6251-9. [PubMed: 18676849]  [MGI Ref ID J:140033]

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Mohan R; Chintala SK; Jung JC; Villar WV; McCabe F; Russo LA; Lee Y; McCarthy BE; Wollenberg KR; Jester JV; Wang M; Welgus HG; Shipley JM; Senior RM; Fini ME. 2002. Matrix metalloproteinase gelatinase B (MMP-9) coordinates and effects epithelial regeneration. J Biol Chem 277(3):2065-72. [PubMed: 11689563]  [MGI Ref ID J:124833]

Nagy V; Bozdagi O; Matynia A; Balcerzyk M; Okulski P; Dzwonek J; Costa RM; Silva AJ; Kaczmarek L; Huntley GW. 2006. Matrix metalloproteinase-9 is required for hippocampal late-phase long-term potentiation and memory. J Neurosci 26(7):1923-34. [PubMed: 16481424]  [MGI Ref ID J:105763]

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Nishikii H; Eto K; Tamura N; Hattori K; Heissig B; Kanaji T; Sawaguchi A; Goto S; Ware J; Nakauchi H. 2008. Metalloproteinase regulation improves in vitro generation of efficacious platelets from mouse embryonic stem cells. J Exp Med 205(8):1917-27. [PubMed: 18663123]  [MGI Ref ID J:138214]

Noble LJ; Donovan F; Igarashi T; Goussev S; Werb Z. 2002. Matrix metalloproteinases limit functional recovery after spinal cord injury by modulation of early vascular events. J Neurosci 22(17):7526-35. [PubMed: 12196576]  [MGI Ref ID J:124001]

Nuki Y; Tsou TL; Kurihara C; Kanematsu M; Kanematsu Y; Hashimoto T. 2009. Elastase-induced intracranial aneurysms in hypertensive mice. Hypertension 54(6):1337-44. [PubMed: 19884566]  [MGI Ref ID J:177972]

Ohki M; Ohki Y; Ishihara M; Nishida C; Tashiro Y; Akiyama H; Komiyama H; Lund LR; Nitta A; Yamada K; Zhu Z; Ogawa H; Yagita H; Okumura K; Nakauchi H; Werb Z; Heissig B; Hattori K. 2010. Tissue type plasminogen activator regulates myeloid-cell dependent neoangiogenesis during tissue regeneration. Blood 115(21):4302-12. [PubMed: 20110420]  [MGI Ref ID J:160268]

Ortega N; Behonick DJ; Colnot C; Cooper DN; Werb Z. 2005. Galectin-3 is a downstream regulator of matrix metalloproteinase-9 function during endochondral bone formation. Mol Biol Cell 16(6):3028-39. [PubMed: 15800063]  [MGI Ref ID J:100747]

Ortega N; Wang K; Ferrara N; Werb Z; Vu TH. 2010. Complementary interplay between matrix metalloproteinase-9, vascular endothelial growth factor and osteoclast function drives endochondral bone formation. Dis Model Mech 3(3-4):224-35. [PubMed: 20142327]  [MGI Ref ID J:160852]

Ovechkin AV; Tyagi N; Rodriguez WE; Hayden MR; Moshal KS; Tyagi SC. 2005. Role of matrix metalloproteinase-9 in endothelial apoptosis in chronic heart failure in mice. J Appl Physiol 99(6):2398-405. [PubMed: 16081621]  [MGI Ref ID J:116865]

Page K; Ledford JR; Zhou P; Wills-Karp M. 2009. A TLR2 agonist in German cockroach frass activates MMP-9 release and is protective against allergic inflammation in mice. J Immunol 183(5):3400-8. [PubMed: 19667087]  [MGI Ref ID J:151856]

Park SJ; Wiekowski MT; Lira SA; Mehrad B. 2006. Neutrophils regulate airway responses in a model of fungal allergic airways disease. J Immunol 176(4):2538-45. [PubMed: 16456015]  [MGI Ref ID J:129184]

Perez SE; Cano DA; Dao-Pick T; Rougier JP; Werb Z; Hebrok M. 2005. Matrix metalloproteinases 2 and 9 are dispensable for pancreatic islet formation and function in vivo. Diabetes 54(3):694-701. [PubMed: 15734845]  [MGI Ref ID J:105134]

Pflugfelder SC; Farley W; Luo L; Chen LZ; de Paiva CS; Olmos LC; Li DQ; Fini ME. 2005. Matrix metalloproteinase-9 knockout confers resistance to corneal epithelial barrier disruption in experimental dry eye. Am J Pathol 166(1):61-71. [PubMed: 15632000]  [MGI Ref ID J:95266]

Pyo R; Lee JK; Shipley JM; Curci JA; Mao D; Ziporin SJ; Ennis TL; Shapiro SD; Senior RM; Thompson RW. 2000. Targeted gene disruption of matrix metalloproteinase-9 (gelatinase B) suppresses development of experimental abdominal aortic aneurysms [see comments] J Clin Invest 105(11):1641-9. [PubMed: 10841523]  [MGI Ref ID J:62760]

Ratzinger G; Stoitzner P; Ebner S; Lutz MB; Layton GT; Rainer C; Senior RM; Shipley JM; Fritsch P; Schuler G; Romani N. 2002. Matrix metalloproteinases 9 and 2 are necessary for the migration of Langerhans cells and dermal dendritic cells from human and murine skin. J Immunol 168(9):4361-71. [PubMed: 11970978]  [MGI Ref ID J:76157]

Renckens R; Roelofs JJ; Florquin S; de Vos AF; Lijnen HR; van't Veer C; van der Poll T. 2006. Matrix metalloproteinase-9 deficiency impairs host defense against abdominal sepsis. J Immunol 176(6):3735-41. [PubMed: 16517742]  [MGI Ref ID J:129550]

Robertson JV; Siwakoti A; West-Mays JA. 2013. Altered expression of transforming growth factor beta 1 and matrix metalloproteinase-9 results in elevated intraocular pressure in mice. Mol Vis 19:684-95. [PubMed: 23559862]  [MGI Ref ID J:196164]

Sabeh F; Li XY; Saunders TL; Rowe RG; Weiss SJ. 2009. Secreted versus membrane-anchored collagenases: relative roles in fibroblast-dependent collagenolysis and invasion. J Biol Chem 284(34):23001-11. [PubMed: 19542530]  [MGI Ref ID J:153449]

Sahay B; Singh A; Gnanamani A; Patsey RL; Blalock JE; Sellati TJ. 2011. CD14 signaling reciprocally controls collagen deposition and turnover to regulate the development of lyme arthritis. Am J Pathol 178(2):724-34. [PubMed: 21281805]  [MGI Ref ID J:169078]

Senft AP; Korfhagen TR; Whitsett JA; Shapiro SD; LeVine AM. 2005. Surfactant protein-D regulates soluble CD14 through matrix metalloproteinase-12. J Immunol 174(8):4953-9. [PubMed: 15814723]  [MGI Ref ID J:98168]

Shubayev VI; Angert M; Dolkas J; Campana WM; Palenscar K; Myers RR. 2006. TNFalpha-induced MMP-9 promotes macrophage recruitment into injured peripheral nerve. Mol Cell Neurosci 31(3):407-15. [PubMed: 16297636]  [MGI Ref ID J:106877]

Stickens D; Behonick DJ; Ortega N; Heyer B; Hartenstein B; Yu Y; Fosang AJ; Schorpp-Kistner M; Angel P; Werb Z. 2004. Altered endochondral bone development in matrix metalloproteinase 13-deficient mice. Development 131(23):5883-95. [PubMed: 15539485]  [MGI Ref ID J:94460]

Stowe AM; Adair-Kirk TL; Gonzales ER; Perez RS; Shah AR; Park TS; Gidday JM. 2009. Neutrophil elastase and neurovascular injury following focal stroke and reperfusion. Neurobiol Dis 35(1):82-90. [PubMed: 19393318]  [MGI Ref ID J:150458]

Su J; Palen DI; Lucchesi PA; Matrougui K. 2006. Mice lacking the gene encoding for MMP-9 and resistance artery reactivity. Biochem Biophys Res Commun 349(4):1177-81. [PubMed: 16979597]  [MGI Ref ID J:113095]

Sullivan BP; Kassel KM; Jone A; Flick MJ; Luyendyk JP. 2012. Fibrin(ogen)-Independent Role of Plasminogen Activators in Acetaminophen-Induced Liver Injury. Am J Pathol 180(6):2321-9. [PubMed: 22507835]  [MGI Ref ID J:184692]

Suofu Y; Clark JF; Broderick JP; Kurosawa Y; Wagner KR; Lu A. 2012. Matrix metalloproteinase-2 or -9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion. Neuroscience 212:180-9. [PubMed: 22521821]  [MGI Ref ID J:184676]

Suzuki Y; Nagai N; Umemura K; Collen D; Lijnen HR. 2007. Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice. J Thromb Haemost 5(8):1732-9. [PubMed: 17596135]  [MGI Ref ID J:148570]

Svedin P; Hagberg H; Savman K; Zhu C; Mallard C. 2007. Matrix metalloproteinase-9 gene knock-out protects the immature brain after cerebral hypoxia-ischemia. J Neurosci 27(7):1511-8. [PubMed: 17301159]  [MGI Ref ID J:141740]

Takabayshi K; Corr M; Hayashi T; Redecke V; Beck L; Guiney D; Sheppard D; Raz E. 2006. Induction of a homeostatic circuit in lung tissue by microbial compounds. Immunity 24(4):475-87. [PubMed: 16618605]  [MGI Ref ID J:113350]

Taylor JL; Hattle JM; Dreitz SA; Troudt JM; Izzo LS; Basaraba RJ; Orme IM; Matrisian LM; Izzo AA. 2006. Role for Matrix Metalloproteinase 9 in Granuloma Formation during Pulmonary Mycobacterium tuberculosis Infection. Infect Immun 74(11):6135-44. [PubMed: 16982845]  [MGI Ref ID J:113558]

Thiolloy S; Halpern J; Holt GE; Schwartz HS; Mundy GR; Matrisian LM; Lynch CC. 2009. Osteoclast-derived matrix metalloproteinase-7, but not matrix metalloproteinase-9, contributes to tumor-induced osteolysis. Cancer Res 69(16):6747-55. [PubMed: 19679556]  [MGI Ref ID J:151928]

Tian L; Stefanidakis M; Ning L; Van Lint P; Nyman-Huttunen H; Libert C; Itohara S; Mishina M; Rauvala H; Gahmberg CG. 2007. Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage. J Cell Biol 178(4):687-700. [PubMed: 17682049]  [MGI Ref ID J:150623]

Tian W; Kyriakides TR. 2009. Matrix metalloproteinase-9 deficiency leads to prolonged foreign body response in the brain associated with increased IL-1beta levels and leakage of the blood-brain barrier. Matrix Biol 28(3):148-59. [PubMed: 19264129]  [MGI Ref ID J:148956]

Ulyanova T; Priestley GV; Banerjee ER; Papayannopoulou T. 2007. Unique and redundant roles of alpha4 and beta2 integrins in kinetics of recruitment of lymphoid vs myeloid cell subsets to the inflamed peritoneum revealed by studies of genetically deficient mice. Exp Hematol 35(8):1256-65. [PubMed: 17553614]  [MGI Ref ID J:126483]

Urbich C; Heeschen C; Aicher A; Sasaki K; Bruhl T; Farhadi MR; Vajkoczy P; Hofmann WK; Peters C; Pennacchio LA; Abolmaali ND; Chavakis E; Reinheckel T; Zeiher AM; Dimmeler S. 2005. Cathepsin L is required for endothelial progenitor cell-induced neovascularization. Nat Med 11(2):206-13. [PubMed: 15665831]  [MGI Ref ID J:99594]

Vaillant C; Meissirel C; Mutin M; Belin MF; Lund LR; Thomasset N. 2003. MMP-9 deficiency affects axonal outgrowth, migration, and apoptosis in the developing cerebellum. Mol Cell Neurosci 24(2):395-408. [PubMed: 14572461]  [MGI Ref ID J:126201]

Vermaelen KY; Cataldo D; Tournoy K; Maes T; Dhulst A; Louis R; Foidart JM; Noel A; Pauwels R. 2003. Matrix metalloproteinase-9-mediated dendritic cell recruitment into the airways is a critical step in a mouse model of asthma. J Immunol 171(2):1016-22. [PubMed: 12847275]  [MGI Ref ID J:84293]

Vu TH; Shipley JM; Bergers G; Berger JE; Helms JA; Hanahan D; Shapiro SD; Senior RM; Werb Z. 1998. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. Cell 93(3):411-22. [PubMed: 9590175]  [MGI Ref ID J:47297]

Wang CH; Anderson N; Li SH; Szmitko PE; Cherng WJ; Fedak PW; Fazel S; Li RK; Yau TM; Weisel RD; Stanford WL; Verma S. 2006. Stem cell factor deficiency is vasculoprotective: unraveling a new therapeutic potential of imatinib mesylate. Circ Res 99(6):617-25. [PubMed: 16931795]  [MGI Ref ID J:125065]

Wang G; Guo Q; Hossain M; Fazio V; Zeynalov E; Janigro D; Mayberg MR; Namura S. 2009. Bone marrow-derived cells are the major source of MMP-9 contributing to blood-brain barrier dysfunction and infarct formation after ischemic stroke in mice. Brain Res 1294:183-92. [PubMed: 19646426]  [MGI Ref ID J:157206]

Wang M; Qin X; Mudgett JS; Ferguson TA; Senior RM; Welgus HG. 1999. Matrix metalloproteinase deficiencies affect contact hypersensitivity: stromelysin-1 deficiency prevents the response and gelatinase B deficiency prolongs the response. Proc Natl Acad Sci U S A 96(12):6885-9. [PubMed: 10359808]  [MGI Ref ID J:55723]

Wang P; Dai J; Bai F; Kong KF; Wong SJ; Montgomery RR; Madri JA; Fikrig E. 2008. Matrix metalloproteinase 9 facilitates West Nile virus entry into the brain. J Virol 82(18):8978-85. [PubMed: 18632868]  [MGI Ref ID J:153406]

Wang X; Jung J; Asahi M; Chwang W; Russo L; Moskowitz MA; Dixon CE; Fini ME; Lo EH. 2000. Effects of matrix metalloproteinase-9 gene knock-out on morphological and motor outcomes after traumatic brain injury. J Neurosci 20(18):7037-42. [PubMed: 10995849]  [MGI Ref ID J:79422]

Wang X; Zhou Y; Tan R; Xiong M; He W; Fang L; Wen P; Jiang L; Yang J. 2010. Mice lacking the matrix metalloproteinase-9 gene reduce renal interstitial fibrosis in obstructive nephropathy. Am J Physiol Renal Physiol 299(5):F973-82. [PubMed: 20844022]  [MGI Ref ID J:165577]

Warner RL; Beltran L; Younkin EM; Lewis CS; Weiss SJ; Varani J; Johnson KJ. 2001. Role of stromelysin 1 and gelatinase B in experimental acute lung injury. Am J Respir Cell Mol Biol 24(5):537-44. [PubMed: 11350822]  [MGI Ref ID J:114188]

West MA; Prescott AR; Chan KM; Zhou Z; Rose-John S; Scheller J; Watts C. 2008. TLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent. J Cell Biol 182(5):993-1005. [PubMed: 18762577]  [MGI Ref ID J:138782]

Xiong W; Knispel R; MacTaggart J; Greiner TC; Weiss SJ; Baxter BT. 2009. Membrane-type 1 matrix metalloproteinase regulates macrophage-dependent elastolytic activity and aneurysm formation in vivo. J Biol Chem 284(3):1765-71. [PubMed: 19010778]  [MGI Ref ID J:145884]

Xu B; Chen H; Xu W; Zhang W; Buckley S; Zheng SG; Warburton D; Kolb M; Gauldie J; Shi W. 2012. Molecular mechanisms of MMP9 overexpression and its role in emphysema pathogenesis of Smad3-deficient mice. Am J Physiol Lung Cell Mol Physiol 303(2):L89-96. [PubMed: 22610349]  [MGI Ref ID J:191358]

Xu J; Mora A; Shim H; Stecenko A; Brigham KL; Rojas M. 2007. Role of the SDF-1/CXCR4 axis in the pathogenesis of lung injury and fibrosis. Am J Respir Cell Mol Biol 37(3):291-9. [PubMed: 17463394]  [MGI Ref ID J:138491]

Xu J; Park PW; Kheradmand F; Corry DB. 2005. Endogenous attenuation of allergic lung inflammation by syndecan-1. J Immunol 174(9):5758-65. [PubMed: 15843578]  [MGI Ref ID J:98401]

Xue M; Hollenberg MD; Yong VW. 2006. Combination of thrombin and matrix metalloproteinase-9 exacerbates neurotoxicity in cell culture and intracerebral hemorrhage in mice. J Neurosci 26(40):10281-91. [PubMed: 17021183]  [MGI Ref ID J:112950]

Yabluchanskiy A; Ma Y; Chiao YA; Lopez EF; Voorhees AP; Toba H; Hall ME; Han HC; Lindsey ML; Jin YF. 2014. Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction. Am J Physiol Heart Circ Physiol 306(10):H1398-407. [PubMed: 24658018]  [MGI Ref ID J:211679]

Yan B; Wei JJ; Yuan Y; Sun R; Li D; Luo J; Liao SJ; Zhou YH; Shu Y; Wang Q; Zhang GM; Feng ZH. 2013. IL-6 cooperates with G-CSF to induce protumor function of neutrophils in bone marrow by enhancing STAT3 activation. J Immunol 190(11):5882-93. [PubMed: 23630344]  [MGI Ref ID J:204780]

Yen JH; Khayrullina T; Ganea D. 2008. PGE2-induced metalloproteinase-9 is essential for dendritic cell migration. Blood 111(1):260-70. [PubMed: 17925490]  [MGI Ref ID J:130104]

Yepes M; Sandkvist M; Moore EG; Bugge TH; Strickland DK; Lawrence DA. 2003. Tissue-type plasminogen activator induces opening of the blood-brain barrier via the LDL receptor-related protein. J Clin Invest 112(10):1533-40. [PubMed: 14617754]  [MGI Ref ID J:119309]

Yin KJ; Cirrito JR; Yan P; Hu X; Xiao Q; Pan X; Bateman R; Song H; Hsu FF; Turk J; Xu J; Hsu CY; Mills JC; Holtzman DM; Lee JM. 2006. Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism. J Neurosci 26(43):10939-48. [PubMed: 17065436]  [MGI Ref ID J:114690]

Zajac E; Schweighofer B; Kupriyanova TA; Juncker-Jensen A; Minder P; Quigley JP; Deryugina EI. 2013. Angiogenic capacity of M1- and M2-polarized macrophages is determined by the levels of TIMP-1 complexed with their secreted proMMP-9. Blood 122(25):4054-67. [PubMed: 24174628]  [MGI Ref ID J:207707]

Zeisberg M; Khurana M; Rao VH; Cosgrove D; Rougier JP; Werner MC; Shield CF 3rd; Werb Z; Kalluri R. 2006. Stage-specific action of matrix metalloproteinases influences progressive hereditary kidney disease. PLoS Med 3(4):e100. [PubMed: 16509766]  [MGI Ref ID J:134125]

Zhang L; Ikegami M; Korfhagen TR; McCormack FX; Yoshida M; Senior RM; Shipley JM; Shapiro SD; Whitsett JA. 2006. Neither SP-A nor NH2-terminal domains of SP-A can substitute for SP-D in regulation of alveolar homeostasis. Am J Physiol Lung Cell Mol Physiol 291(2):L181-90. [PubMed: 16500946]  [MGI Ref ID J:121212]

Zhong Q; Kowluru RA. 2013. Regulation of matrix metalloproteinase-9 by epigenetic modifications and the development of diabetic retinopathy. Diabetes 62(7):2559-68. [PubMed: 23423566]  [MGI Ref ID J:208549]

van Deventer HW; Palmieri DA; Wu QP; McCook EC; Serody JS. 2013. Circulating Fibrocytes Prepare the Lung for Cancer Metastasis by Recruiting Ly-6C+ Monocytes Via CCL2. J Immunol 190(9):4861-7. [PubMed: 23536638]  [MGI Ref ID J:195511]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Breeding & HusbandryThis strain originated on a B6;129 background, was mated to Black Swiss mice for an unknown number of generations and crossed to FVB/N mice for five generations. It then was crossed to C57BL/6J mice for at least five generations. Coat color expected from breeding:nonagouti
Mating SystemHomozygote x Homozygote         (Female x Male)   04-JUN-09
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHomozygous for Mmp9tm1Tvu  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for Mmp9tm1Tvu x Homozygous for Mmp9tm1Tvu  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHomozygous for Mmp9tm1Tvu  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for Mmp9tm1Tvu x Homozygous for Mmp9tm1Tvu  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

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