Strain Name:

B6C3Fe a/a-Csf1op/J

Stock Number:

000231

Availability:

Repository- Live

Description

Strain Information

Former Names B6C3Fe-a/a-Csf1op    (Changed: 15-DEC-04 )
Type Mutant Stock;
Additional information on Genetically Engineered Mutant Mice.
Mating SystemOvarian Transplant-Cross-Intercross         (Female x Male)
TJL Breeding Summary: homozygous ovarian transplant x B6C3Fe a/a F1 then obligate heterozygote x heterozygote
Specieslaboratory mouse
GenerationN57F2 (09-JAN-07)

Appearance
black, osteopetrosis
Related Genotype: a/a Csf1op/Csf1op

black, unaffected
Related Genotype: a/a Csf1op/+ or a/a ?/+

Description
Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.

Control Information

  Control
   Untyped from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   a allele
003879   B10;TFLe-a/a T tf/+ tf/J
001538   B6 x B6C3Sn a/A-T(1;9)27H/J
000916   B6 x B6C3Sn a/A-T(5;12)31H/J
000602   B6 x B6C3Sn a/A-T(8;16)17H/J
000618   B6 x FSB/GnEi a/a Ctslfs/J
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000601   B6 x STOCK a/a T(7;18)50H/J
000592   B6 x STOCK T(2;4)13H a/J
000001   B6.C3 A/a Mgrn1md/J
000785   B6;D2-a Es1e/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
002807   B6C3Fe a/a-Meox2fla/J
000224   B6C3Fe a/a-Scyl1mdf/J
001037   B6C3Fe a/a-Agtpbp1pcd/J
000221   B6C3Fe a/a-Alx4lst-J/J
002062   B6C3Fe a/a-Atp7aMo-8J/J
001756   B6C3Fe a/a-Cacng2stg/J
001815   B6C3Fe a/a-Col1a2oim/J
000209   B6C3Fe a/a-Dh/J
000211   B6C3Fe a/a-Dstdt-J/J
000210   B6C3Fe a/a-Edardl-J/J
000207   B6C3Fe a/a-Edaraddcr/J
000182   B6C3Fe a/a-Eef1a2wst/J
001278   B6C3Fe a/a-Glra1spd/J
000241   B6C3Fe a/a-Glrbspa/J
002875   B6C3Fe a/a-Hoxd13spdh/J
000304   B6C3Fe a/a-Krt71Ca Scn8amed-J/J
000226   B6C3Fe a/a-Largemyd/J
000636   B6C3Fe a/a-Lmx1adr-J/J
001280   B6C3Fe a/a-Lse/J
001573   B6C3Fe a/a-MitfMi/J
001035   B6C3Fe a/a-Napahyh/J
000181   B6C3Fe a/a-Otogtwt/J
000278   B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J
000205   B6C3Fe a/a-Papss2bm/J
002078   B6C3Fe a/a-Pcdh15av-2J/J
000246   B6C3Fe a/a-Pitpnavb/J
001430   B6C3Fe a/a-Ptch1mes/J
000506   B6C3Fe a/a-Qkqk/J
000235   B6C3Fe a/a-Relnrl/J
000237   B6C3Fe a/a-Rorasg/J
000290   B6C3Fe a/a-Sox10Dom/J
000230   B6C3Fe a/a-Tcirg1oc/J
003612   B6C3Fe a/a-Trak1hyrt/J
001512   B6C3Fe a/a-Ttnmdm/J
001607   B6C3Fe a/a-Unc5crcm/J
000005   B6C3Fe a/a-Wc/J
000243   B6C3Fe a/a-Wnt1sw/J
000248   B6C3Fe a/a-Xpl/J
001750   B6C3Fe a/a-XsJ/J
000624   B6C3Fe a/a-anx/J
003020   B6C3Fe a/a-dep/J
002018   B6C3Fe a/a-din/J
002339   B6C3Fe a/a-nma/J
000240   B6C3Fe a/a-soc/J
000063   B6C3Fe a/a-sy/J
001055   B6C3Fe a/a-tip/J
000245   B6C3Fe a/a-tn/J
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/a
000971   B6EiC3 a/A-Och/J
000551   B6EiC3 a/A-Tbx15de-H/J
006450   B6EiC3 a/A-Vss/J
000557   B6EiC3-+ a/LnpUl A/J
000503   B6EiC3Sn a/A-Gy/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
000391   B6EiC3Sn a/A-Pax6Sey-Dey/J
001924   B6EiC3Sn a/A-Ts(1716)65Dn
001923   B6EiC3Sn a/A-Ts(417)2Lws Tim/J
000225   C3FeLe.B6 a/a-Ptpn6me/J
008425   C3FeLe.B6-a Trl/J
000198   C3FeLe.B6-a/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
001886   C3HeB/FeJLe a/a-gnd/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
001057   HPT/LeJ
000260   JGBF/LeJ
000265   MY/HuLeJ
000308   SSL/LeJ
000994   STOCK a Myo5ad Mregdsu/J
000064   STOCK a Tyrp1b Sisi/J
002238   STOCK a Tyrp1b shmy/J
001433   STOCK a skt/J
000579   STOCK a tp/J
000319   STOCK a us/J
002648   STOCK a/a Cln6nclf/J
000317   STOCK a/a Egfrwa2/J
000302   STOCK a/a MitfMi-wh +/+ Itpr1opt/J
000286   STOCK a/a Myo5ad fd/+ +/J
000206   STOCK a/a Tyrc-h/J
001432   STOCK a/a Tyrp1b sks/Tyrp1b +/J
000281   STOCK a/a ma ft/ma ft/J
000312   STOCK stb + a/+ Fignfi a/J
000596   STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J
000970   STOCK T(2;16)28H A/T(2;16)28H a/J
000590   STOCK T(2;4)1Sn a/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
000623   TR/DiEiJ
View Strains carrying   a     (103 strains)

Strains carrying other alleles of a
003301   (C57BL/6J x C3H-Eya1bor)F1/J
000251   AEJ.Cg-ae +/a Gdf5bp-H/J
000202   AEJ/Gn-bd/J
000199   AEJ/GnLeJ
000427   B10.CE-H13b Aw/(30NX)SnJ
000420   B10.LP-H13b Aw/Sn
000477   B10.PA-Pldnpa H3e at/SnJ
000419   B10.UW-H3b we Pax1un at/SnJ
000593   B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000599   B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
000507   B6 x B6EiC3 a/A-Otcspf/J
002016   B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ
000552   B6-Aw-J-EdaTa-6J.Cg-Sxr
001730   B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J
000841   B6-Aw-J.CBy-EdaTa-By/J
001809   B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J
000600   B6-Gpi1b x B6CBCa Aw-J/A-T(7;15)9H Gpi1a/J
000769   B6.C/(HZ18)By-at-44J/J
000203   B6.C3-Aiy/a/J
001572   B6.C3-am-J/J
000017   B6.C3Fe-Avy/J
000628   B6.CE-A Amy1b Amy2b/J
005505   B6.Cg-Ay Slc7a11sut/LmLlp
000021   B6.Cg-Ay/J
100409   B6129PF1/J-Aw-J/Aw
004200   B6;CBACa Aw-J/A-Npr2cn-2J/J
000505   B6C3 Aw-J/A-Mutedmu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
000065   B6C3Fe a/a-we Pax1un at/J
000314   B6CBACa Aw-J/A-EdaTa/J-XO
000501   B6CBACa Aw-J/A-Aifm1Hq/J
001046   B6CBACa Aw-J/A-Grid2Lc/J
000500   B6CBACa Aw-J/A-Gs/J
002703   B6CBACa Aw-J/A-Hydinhy3/J
000247   B6CBACa Aw-J/A-Kcnj6wv/J
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000515   B6CBACa Aw-J/A-SfnEr/J
000242   B6CBACa Aw-J/A-spc/J
000288   B6CBACa Aw-J/A-we a Mafbkr/J
001201   B6CBACaF1/J-Aw-J/A
001752   B6CBCa Aw-J/A-T(7;15)9H/J
006450   B6EiC3 a/A-Vss/J
000557   B6EiC3-+ a/LnpUl A/J
000504   B6EiC3Sn a/A-Cacnb4lh/J
000553   B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
001923   B6EiC3Sn a/A-Ts(417)2Lws Tim/J
000200   C3FeB6 A/Aw-J-Ankank/J
000638   C3FeB6 A/Aw-J-Spnb4qv-J/J
001203   C3FeB6F1/J A/Aw-J
001272   C3H/HeSnJ-Ahvy/J
000099   C3HeB/FeJ-Avy/J
000338   C57BL/6J Aw-J-EdaTa-6J/J
000258   C57BL/6J-Ai/a/J
000774   C57BL/6J-Asy/a/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
000051   C57BL/6J-Aw-J/J
000055   C57BL/6J-at-33J/J
000070   C57BL/6J-atd/J
002468   KK.Cg-Ay/J
000262   LS/LeJ
000283   LT.CAST-A/J
001759   STOCK A Tyrc Sha/J
001427   STOCK Aw us/J
View Strains carrying other alleles of a     (67 strains)

Additional Web Information

Genetic Quality Control Annual Report

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Osteopetrosis, Autosomal Recessive 1; OPTB1 - Models with phenotypic similarity to human disease where etiologies are distinct.2
2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Csf1op/Csf1op

        B6C3Fe a/a-Csf1op/J
  • lethality-postnatal
  • postnatal lethality (MGI Ref ID J:73663)
    • reduced numbers of homozygotes survive to weaning
  • growth/size phenotype
  • decreased body weight (MGI Ref ID J:104139)
    • low body weight
  • postnatal growth retardation (MGI Ref ID J:73663)
    • slower growth rate
  • immune system phenotype
  • abnormal Kupffer cell morphology (MGI Ref ID J:26978)
    • 30% fewer Kupffer cells than normal littermates
    • irregular distribution of Kupffer cells in liver lobules
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections
  • abnormal microglial cell morphology (MGI Ref ID J:49613)
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes
  • abnormal osteoclast morphology (MGI Ref ID J:26978)
    • reduced size and number of multinuclear osteoclasts
  • abnormal perivascular macrophage morphology (MGI Ref ID J:49613)
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex
  • abnormal spleen cellularity (MGI Ref ID J:104139)
    • increased concentration of CFU-S cells, however , size and differentiation pattern of spleen colonies is normal
    • spleen mostly composed of fibroblastoid cells
    • reduced number of macrophages
    • increased numbers of BFU-E and HPP-CFC
  • abnormal spleen red pulp morphology (MGI Ref ID J:26978)
    • extensive extramedullary hematopoiesis
  • abnormal thymus medulla morphology (MGI Ref ID J:26978)
    • atrophic with numerous macrophages
  • absent Langerhans cell (MGI Ref ID J:112594)
    • absence of Langerhans cells in newborns but numbers recover in adults
  • decreased leukocyte cell number (MGI Ref ID J:104139)
    • decreased macrophage cell number (MGI Ref ID J:26978)
      • decreased numbers of macrophages in liver, spleen, bone marrow, kidney, subcutaneous tissue, uterus and ovary
      • macrophages exhibit intracytoplasmic organelles in splenic, thymic and bone marrow
      • macrophage organelles and microvillous projections are poorly developed
      • decreased numbers in spleen and marrow
    • decreased monocyte cell number (MGI Ref ID J:104139)
      • almost complete absence of monocytes in peripheral blood
  • decreased thymus cortex area (MGI Ref ID J:26978)
    • consists mostly of thymic epithelial cells
  • skeleton phenotype
  • abnormal bone marrow cavity morphology (MGI Ref ID J:26978)
    • reduced numbers of hematopoietic cells
    • excessive amount of bone trabeculae
  • abnormal bone marrow morphology (MGI Ref ID J:73663)
    • femoral bone marrow cellularity is reduced early but recovers to control levels by 8 months of age
  • abnormal cancellous bone morphology (MGI Ref ID J:73663)
    • higher levels of trabecular bone
  • abnormal femur morphology (MGI Ref ID J:26978)
    • distal end is wide, diaphysis does not have a well defined cortex
  • abnormal long bone hypertrophic chondrocyte zone (MGI Ref ID J:26978)
  • abnormal osteoclast morphology (MGI Ref ID J:26978)
    • reduced size and number of multinuclear osteoclasts
  • abnormal tibia morphology (MGI Ref ID J:26978)
    • proximal end is wide, diaphysis does not have a well defined cortex
  • reproductive system phenotype
  • abnormal lactation (MGI Ref ID J:20519)
    • only 10% of females can lactate, however, lactation in this subset is inefficient
  • abnormal mammary gland development (MGI Ref ID J:20519)
    • postpartum females exhibit incompletely differentiated mammary gland tissue with a nonsecretory phenotype
    • alveolar cells are cuboidal, contain large lipid vesicles and the lumen is small or unformed
    • abnormal branching of the mammary ductal tree (MGI Ref ID J:20519)
      • ductal structures are poorly developed with incomplete arborization
    • abnormal mammary gland growth during pregnancy (MGI Ref ID J:20519)
      • lobulo-alveolar development is premature and occupies 56% of mammary gland by day 18 of pregnancy
  • abnormal uterus morphology (MGI Ref ID J:26978)
    • poor development of glandular epithelia
    • abnormal endometrium morphology (MGI Ref ID J:26978)
      • endometrium is hypoplastic
    • abnormal myometrium morphology (MGI Ref ID J:26978)
      • myometrium is hypoplastic
  • increased testis weight (MGI Ref ID J:34371)
    • as a percentage of body weight, testicular tissue is increased over controls
  • oligozoospermia (MGI Ref ID J:34371)
    • epididymal sperm count 60% lower than control
    • percentage of dead sperm is two times higher than control
  • reduced male fertility (MGI Ref ID J:34371)
    • males take 5 times longer to mate than controls
    • males mate on the first night, but not on subsequent nights in timed mating experiments
  • nervous system phenotype
  • abnormal microglial cell morphology (MGI Ref ID J:49613)
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes
  • abnormal summary potential (MGI Ref ID J:19549)
    • total intracortical transmembrane current significantly reduced as measured by intracortical VEP
    • altered neural firing as demonstrated by multiple unit activity (MUA) measurement
  • amyloid beta deposits (MGI Ref ID J:87261)
    • 100 to 200 fibrillar plaques observed in cerebral cortex
    • 20 to 60 plaques observed in amygdala and hypothalamus
    • small number of plaques observed in hippocampus
  • decreased pyramidal neuron number (MGI Ref ID J:87261)
    • hippocampal neuron loss in CA1 and CA3 regions
  • hematopoietic system phenotype
  • abnormal Kupffer cell morphology (MGI Ref ID J:26978)
    • 30% fewer Kupffer cells than normal littermates
    • irregular distribution of Kupffer cells in liver lobules
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections
  • abnormal microglial cell morphology (MGI Ref ID J:49613)
    • reduced numbers of microglial cells in frontal cortex, parietal cortex and corpus callosum
    • microglial cells in frontal cortex have smaller cell bodies and shorter cytoplasmic processes
  • abnormal osteoclast morphology (MGI Ref ID J:26978)
    • reduced size and number of multinuclear osteoclasts
  • abnormal perivascular macrophage morphology (MGI Ref ID J:49613)
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex
  • abnormal spleen cellularity (MGI Ref ID J:104139)
    • increased concentration of CFU-S cells, however , size and differentiation pattern of spleen colonies is normal
    • spleen mostly composed of fibroblastoid cells
    • reduced number of macrophages
    • increased numbers of BFU-E and HPP-CFC
  • abnormal spleen red pulp morphology (MGI Ref ID J:26978)
    • extensive extramedullary hematopoiesis
  • abnormal thymus medulla morphology (MGI Ref ID J:26978)
    • atrophic with numerous macrophages
  • absent Langerhans cell (MGI Ref ID J:112594)
    • absence of Langerhans cells in newborns but numbers recover in adults
  • decreased bone marrow cell number (MGI Ref ID J:104139)
    • number of cells 10 fold less than controls
    • marrow mostly composed of fibroblastoid cells
    • reduced numbers of CFU-S cells
  • decreased leukocyte cell number (MGI Ref ID J:104139)
    • decreased macrophage cell number (MGI Ref ID J:26978)
      • decreased numbers of macrophages in liver, spleen, bone marrow, kidney, subcutaneous tissue, uterus and ovary
      • macrophages exhibit intracytoplasmic organelles in splenic, thymic and bone marrow
      • macrophage organelles and microvillous projections are poorly developed
      • decreased numbers in spleen and marrow
    • decreased monocyte cell number (MGI Ref ID J:104139)
      • almost complete absence of monocytes in peripheral blood
  • decreased thymus cortex area (MGI Ref ID J:26978)
    • consists mostly of thymic epithelial cells
  • extramedullary hematopoiesis (MGI Ref ID J:26978)
    • observed in splenic red pulp
  • liver/biliary system phenotype
  • abnormal Kupffer cell morphology (MGI Ref ID J:26978)
    • 30% fewer Kupffer cells than normal littermates
    • irregular distribution of Kupffer cells in liver lobules
    • Kupffer cells possess phagocytized blood cells, poorly developed organelles and microvilli projections
  • limbs/digits/tail phenotype
  • abnormal femur morphology (MGI Ref ID J:26978)
    • distal end is wide, diaphysis does not have a well defined cortex
  • abnormal tibia morphology (MGI Ref ID J:26978)
    • proximal end is wide, diaphysis does not have a well defined cortex
  • endocrine/exocrine gland phenotype
  • abnormal lactation (MGI Ref ID J:20519)
    • only 10% of females can lactate, however, lactation in this subset is inefficient
  • abnormal mammary gland development (MGI Ref ID J:20519)
    • postpartum females exhibit incompletely differentiated mammary gland tissue with a nonsecretory phenotype
    • alveolar cells are cuboidal, contain large lipid vesicles and the lumen is small or unformed
    • abnormal branching of the mammary ductal tree (MGI Ref ID J:20519)
      • ductal structures are poorly developed with incomplete arborization
    • abnormal mammary gland growth during pregnancy (MGI Ref ID J:20519)
      • lobulo-alveolar development is premature and occupies 56% of mammary gland by day 18 of pregnancy
  • increased testis weight (MGI Ref ID J:34371)
    • as a percentage of body weight, testicular tissue is increased over controls
  • homeostasis/metabolism phenotype
  • decreased circulating testosterone level (MGI Ref ID J:34371)
  • hearing/vestibular/ear phenotype
  • abnormal vestibular system physiology (MGI Ref ID J:19549)
    • poorly formed or absent response to surface visual evoked potential (VEP)
  • decreased brainstem auditory evoked potential (MGI Ref ID J:19549)
    • delayed and diminished response to brainstem auditory evoked potential (BAEP)
  • other phenotype
  • amyloid beta deposits (MGI Ref ID J:87261)
    • 100 to 200 fibrillar plaques observed in cerebral cortex
    • 20 to 60 plaques observed in amygdala and hypothalamus
    • small number of plaques observed in hippocampus
  • cardiovascular system phenotype
  • abnormal perivascular macrophage morphology (MGI Ref ID J:49613)
    • reduced numbers of perivascular macrophages (as identified by F4/80 staining) are found in parietal cortex

Csf1op/Csf1op

        involves: C3HeB/FeJ * C57BL/6J
  • homeostasis/metabolism phenotype
  • abnormal circulating calcium level (MGI Ref ID J:5634)
    • unable to raise serum calcium concentration in response to parathyroid extract (PTE)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Csf1op/Csf1op

        C57BL/6J-Csf1op
  • skeleton phenotype
  • abnormal osteoblast physiology (MGI Ref ID J:5634)
    • increased bone matrix formation to postnatal day 40
    • decreased bone matrix formation after day 81
  • abnormal skeleton morphology (MGI Ref ID J:110981)
    • overall skeleton is smaller than in wild-type
    • abnormal bone structure (MGI Ref ID J:5634)
      • large lipoid masses in vascular and extravascular areas of bone
      • abnormal bone marrow cavity morphology (MGI Ref ID J:5634)
        • delayed development of bone marrow cavity
        • abnormally high numbers of megakaryocytes
      • abnormal cancellous bone morphology (MGI Ref ID J:5634)
        • long bones filled with primary spongiosa
      • abnormal osteoclast morphology (MGI Ref ID J:5634)
        • osteoclasts small and few in number
        • abnormal distribution of acid phosphatase activity
        • decreased osteoclast cell number (MGI Ref ID J:5634)
      • osteopetrosis (MGI Ref ID J:5634)
      • osteoporosis (MGI Ref ID J:110981)
        • mice exhibit osteoporosis
    • domed skull (MGI Ref ID J:5634)
      • observed by 10 days
  • immune system phenotype
  • abnormal osteoclast morphology (MGI Ref ID J:5634)
    • osteoclasts small and few in number
    • abnormal distribution of acid phosphatase activity
    • decreased osteoclast cell number (MGI Ref ID J:5634)
  • abnormal spleen red pulp morphology (MGI Ref ID J:5634)
    • sinusoids less developed
  • decreased macrophage cell number (MGI Ref ID J:110981)
    • cells expressing F4/80+ (a marker for macrophages) are almost entirely absent
    • decreased osteoclast cell number (MGI Ref ID J:5634)
  • hematopoietic system phenotype
  • abnormal osteoclast morphology (MGI Ref ID J:5634)
    • osteoclasts small and few in number
    • abnormal distribution of acid phosphatase activity
    • decreased osteoclast cell number (MGI Ref ID J:5634)
  • abnormal spleen red pulp morphology (MGI Ref ID J:5634)
    • sinusoids less developed
  • decreased macrophage cell number (MGI Ref ID J:110981)
    • cells expressing F4/80+ (a marker for macrophages) are almost entirely absent
    • decreased osteoclast cell number (MGI Ref ID J:5634)
  • reproductive system phenotype
  • reduced fertility (MGI Ref ID J:5634)
  • craniofacial phenotype
  • abnormal snout morphology (MGI Ref ID J:110981)
    • snouts are rounded
  • absent incisors (MGI Ref ID J:5634)
    • absence of incisors is observed by 10 days
  • absent teeth (MGI Ref ID J:110981)
    • homozygous mice are toothless
  • domed skull (MGI Ref ID J:5634)
    • observed by 10 days
  • life span-post-weaning/aging
  • premature death (MGI Ref ID J:5634)
    • 40% of mice that survive weaning die by 12 months
    • hydrocephalus is observed in mice that die at an early age
  • limbs/digits/tail phenotype
  • abnormal paw/hand/foot morphology (MGI Ref ID J:5634)
    • all hind foot digits curve progressively laterally or medially
    • change in shape of hind feet during growth, first digit of hindfoot often becomes parallel to the second digit
  • short limbs (MGI Ref ID J:5634)
  • short tail (MGI Ref ID J:5634)
    • frequent development of s-type curves
  • growth/size phenotype
  • postnatal slow weight gain (MGI Ref ID J:5634)
    • from day 10 weight gain does not match control
  • endocrine/exocrine gland phenotype
  • abnormal thyroid parafollicular C-cells (MGI Ref ID J:5634)
    • parafollicular cell density in thyroid is significantly increased during first three months
  • homeostasis/metabolism phenotype
  • hypophosphatemia (MGI Ref ID J:5634)
    • serum phosphate levels average 30% below control

Csf1op/Csf1op

        Background Not Specified
  • reproductive system phenotype
  • abnormal ovary morphology (MGI Ref ID J:38039)
    • very few macrophages present in ovaries at all stages of cycle and follicular development
  • decreased ovulation frequency (MGI Ref ID J:38039)
    • 20% of ovaries fail to undergo ovulation
    • ovulation rate low for mice that do ovulate
  • prolonged estrous cycle (MGI Ref ID J:38039)
    • females reach estrus every 14 days
  • embryogenesis phenotype
  • impaired implantation (MGI Ref ID J:38039)
    • lower number of implantations
  • endocrine/exocrine gland phenotype
  • abnormal ovary morphology (MGI Ref ID J:38039)
    • very few macrophages present in ovaries at all stages of cycle and follicular development
View Research Applications

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

Neurobiology Research
Alzheimer's Disease
Parkinson's Disease

Csf1op related

Cancer Research
Growth Factors/Receptors/Cytokines

Developmental Biology Research
Skeletal Defects (osteopetrosis)

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology and Inflammation Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
Immunodeficiency Associated with Other Defects

Mouse/Human Gene Homologs
Infantile neuronal ceroid lipofuscinosis

Research Tools
Immunology and Inflammation Research (Macrophage Deficiency)

Genes & Alleles

Gene & Allele Information

Allele Symbol Csf1op
Allele Name osteopetrosis
Allele Type Spontaneous
Common Name(s) Csf-1op; Csf1<-> op; Csfmop; M-; csfmop; op;
Strain of OriginC57BL/6J-Pou1f1
Gene Symbol and Name Csf1, colony stimulating factor 1 (macrophage)
Chromosome 3
Gene Common Name(s) C87615; CSF-1; Csfm; M-CSF; MCSF; MGC31930; colony stimulating factor, macrophage; colony-stimulating factor-1; expressed sequence C87615; op; osteopetrosis;
General Note Mutant homozygotes can be recognized at 10 days of age by absence of incisors and by a domed skull. They survive weaning if provided with soft food, but viability is somewhat reduced and breeding performance is very poor (J:5634). The main skeletal defect in Csf1op/Csf1op mice is a severely restricted capacity for bone remodelling, due to a shortage of osteoclasts (J:5634). Osteoclast populations appear normal at birth in mutant animals, but numbers quickly decrease and are almost nil by 3-4 days of age (J:33189). The few osteoclasts present are small and show an abnormal distribution of acid phosphatase (J:5634).

Young homozygotes have excessive accumulations of bone with lack of marrow cavities, increases in bone matrix formation and in parafollicular (calcitonin-secreting) cells of the thyroid, and normal serum calcium but low serum phosphate (J:5634). There is an extremely efficient mechanism for the absorption of dietary calcium in Csf1op homozygous mice, independent of vitamin D. Serum calcium remains at normal levels, however, due to rapid incorporation of the absorbed calcium into bone (J:31874). The skeletal signs of the disease slowly disappear beginning at 6 weeks, when bone matrix formation beginsto change from above normal (145% of normal) to below normal (20% of normal). Bone remodelling capacity, though reduced, is able, combined with the decline in rate of bone formation, to remove excess skeletal mass to produce nearly normal bones in older animals (J:5634). The lack of osteoclasts can be cured by daily injections of exogenous M-CSF; even a single M-CSF injection can recruit functional osteoclasts (J:4732). The effect of M-CSF appears to be on differentiation of osteoclasts rather than on proliferation of osteoclast precursors (J:12210).

Cranial flat bone formation in the Csf1op/Csf1op mouse is abnormal (J:18356). The masseter muscle of these mutant mice shows postnatal changes, probably due to failure to produceteeth and the resulting reduction in development of periodontal ligaments (J:20589).Occlusion of the marrow cavities in young Csf1op/Csf1op mice leads to reduced hemopoiesis in the marrow, accompanied by splenomegaly and prolongedsplenic hemopoiesis. The bone marrow is, however, seeded with the requisite hemopoietic precursor cells; and the reduced hemopoiesis in marrow is not due to direct effects of M-CSF (J:19549). Macrophage populations derived from monocytes are absent in Csf1op homozygotes, but mature macrophages are produced from other precursors under the influence of granulocyte-macrophage colony stimulating factor (GM-CSF) (J:26978).

Bone marrow macrophages arrest in G1 phase in M-CSF deficient mice; thefactor regulates cyclins involved in commitment of cells to S phase (J:14776). Bacterial translocation and lipopolysaccharide-induced morbidity and mortality are no different in Csf1op/Csf1op mice than in normal littermates (J:20379). Low levels of cytokines involved in immune reactions, found in 6 week old Csf1op homozygotes, recover to normal in these mice at older ages, as the bone marrow macrophage population is restored to normal (J:18531). Macrophage deficiencies inCsf1op/Csf1op mutants do not prevent them mounting normal T cell responses to infection (J:24207).

Intramuscular transplantation of myoblasts capable of producing M-CSF into Csf1op homozygotes introduces the factor into the circulation of the mutant mice along with macrophages, but only transiently. The induced M-CSF may have been bound by macrophages accumulating at the site of the transplant. Macrophages accumulate at the site of muscle damage due to transplantation or to control muscle insult, and the damage can be repaired in the osteopetrotic mice (J:38812).

The low pregnancy rates and reduced litter sizes among Csf1op/Csf1op female mice arise from disruption of estrous cycles and ofovulation. Estrus cycle length is lengthened in these mice (J:38039). Numbers of ovulated ova in Fallopian tubules are decreased in mutant mice relative to wild-type. Antral and mature follicles in the proestrous ovary are also decreased, and the proliferative capacity of granulosa ccells in antral follicules is reduced, as are numbers of granulosa cells and macrophages. All of these functions can be increased by daily treatment with M-CSF (J:30863). Male mutant animals experience lowered levels of both circulating and testicular testosterone, accompanied by reduced mating capacity and lowered numbers of viable sperm (J:34371). Csf1op/Csf1op females also are incapable of feeding any pups they may bear. Mammary gland ductal growth is incomplete during pregnancy, and the mice fail to switch to a lactational state after parturition, despite the presence of milk proteins (J:20519).

Brain cytoarchitectural abnormalities are not found in Csf1op homozygotes (J:19249), and microglia in these mice are normal in number and morphology (J:23600). Vulnerability of neurons to ischemic injury is increased, and the microglial response to neuronal injury reduced, in Csf1op homozygotes (J:30212). Electrophysiologicassay of mutant mice revealed abnormal auditory and visual evoked potentials and other signs of aberrant neuronal function (J:35818). Epidermal Langerhans cells (J:3186) and nonlymphoid dendritic cells in lymphoid tissues and skin (J:4355) differentiate normally in Csf1op/Csf1op mice.

In two studies of Apoe mutant mice also carrying Csf1op, atherotic lesions of the proximal aorta were abolished or significantly reduced in size relative to Apoe mutants homozygous for the normal allele at Csf1 (J:40136, J:29024). The results may have been due to reduced macrophages or M-CSF, but were not due to reductions in circulating lipoprotein (J:40136).

Molecular Note A single nucleotide (T) insertion 262 bp downstream from the initiation codon resulted in a frameshift and the creation of a stop codon 21 bp dowstream of the insertion. [MGI Ref ID J:10519]
 
Allele Symbol a
Allele Name nonagouti
Allele Type Spontaneous

Genotyping

Genotyping Information

Genotyping Protocols

Csf1op, HRM, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

Bruhns P; Samuelsson A; Pollard JW; Ravetch JV. 2003. Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease. Immunity 18(4):573-81. [PubMed: 12705859]  [MGI Ref ID J:83013]

Ida-Yonemochi H; Noda T; Shimokawa H; Saku T. 2002. Disturbed tooth eruption in osteopetrotic (op/op) mice: histopathogenesis of tooth malformation and odontomas. J Oral Pathol Med 31(6):361-73. [PubMed: 12201247]  [MGI Ref ID J:78487]

Kaku M; Tsutsui K; Motokawa M; Kawata T; Fujita T; Kohno S; Tohma Y; Ohtani J; Tenjoh K; Tanne K. 2003. Amyloid beta protein deposition and neuron loss in osteopetrotic (op/op) mice. Brain Res Brain Res Protoc 12(2):104-8. [PubMed: 14613812]  [MGI Ref ID J:87261]

Lenda DM; Kikawada E; Stanley ER; Kelley VR. 2003. Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation. J Immunol 170(6):3254-62. [PubMed: 12626584]  [MGI Ref ID J:82301]

Lenda DM; Stanley ER; Kelley VR. 2004. Negative role of colony-stimulating factor-1 in macrophage, T cell, and B cell mediated autoimmune disease in MRL-Fas(lpr) mice. J Immunol 173(7):4744-54. [PubMed: 15383612]  [MGI Ref ID J:93714]

Naito M; Hayashi S; Yoshida H; Nishikawa S; Shultz LD; Takahashi K. 1991. Abnormal differentiation of tissue macrophage populations in 'osteopetrosis' (op) mice defective in the production of macrophage colony-stimulating factor. Am J Pathol 139(3):657-67. [PubMed: 1887865]  [MGI Ref ID J:26978]

Sasaki A; Yokoo H; Naito M; Kaizu C; Shultz LD; Nakazato Y. 2000. Effects of macrophage-colony-stimulating factor deficiency on the maturation of microglia and brain macrophages and on their expression of scavenger receptor. Neuropathology 20(2):134-42. [PubMed: 10935450]  [MGI Ref ID J:82594]

Tagaya H; Kunisada T; Yamazaki H; Yamane T; Tokuhisa T; Wagner EF; Sudo T; Shultz LD; Hayashi SI. 2000. Intramedullary and extramedullary B lymphopoiesis in osteopetrotic mice. Blood 95(11):3363-70. [PubMed: 10828017]  [MGI Ref ID J:82593]

Yoshida H; Hayashi S; Kunisada T; Ogawa M; Nishikawa S; Okamura H; Sudo T; Shultz LD; Nishikawa S. 1990. The murine mutation osteopetrosis is in the coding region of the macrophage colony stimulating factor gene. Nature 345(6274):442-4. [PubMed: 2188141]  [MGI Ref ID J:10519]

Csf1op related

Abboud SL; Woodruff K; Liu C; Shen V; Ghosh-Choudhury N. 2002. Rescue of the osteopetrotic defect in op/op mice by osteoblast-specific targeting of soluble colony-stimulating factor-1. Endocrinology 143(5):1942-9. [PubMed: 11956177]  [MGI Ref ID J:76327]

Alnaeeli M; Penninger JM; Teng YT. 2006. Immune interactions with CD4+ T cells promote the development of functional osteoclasts from murine CD11c+ dendritic cells. J Immunol 177(5):3314-26. [PubMed: 16920972]  [MGI Ref ID J:139526]

Araki M; Fukumatsu Y; Katabuchi H; Shultz LD; Takahashi K; Okamura H. 1996. Follicular development and ovulation in macrophage colony-stimulating factor-deficient mice homozygous for the osteopetrosis (op) mutation. Biol Reprod 54(2):478-84. [PubMed: 8788202]  [MGI Ref ID J:30863]

Banaei-Bouchareb L; Gouon-Evans V; Samara-Boustani D; Castellotti MC; Czernichow P; Pollard JW; Polak M. 2004. Insulin cell mass is altered in Csf1op/Csf1op macrophage-deficient mice. J Leukoc Biol 76(2):359-67. [PubMed: 15178709]  [MGI Ref ID J:91463]

Batchelor PE; Porritt MJ; Nilsson SK; Bertoncello I; Donnan GA; Howells DW. 2002. Periwound dopaminergic sprouting is dependent on numbers of wound macrophages. Eur J Neurosci 15(5):826-32. [PubMed: 11906524]  [MGI Ref ID J:107999]

Begg SK; Radley JM; Pollard JW; Chisholm OT; Stanley ER; Bertoncello I. 1993. Delayed hematopoietic development in osteopetrotic (op/op) mice. J Exp Med 177(1):237-42. [PubMed: 8418205]  [MGI Ref ID J:3480]

Berezovskaya O; Maysinger D; Fedoroff S. 1995. The hematopoietic cytokine, colony-stimulating factor 1, is also a growth factor in the CNS: congenital absence of CSF-1 in mice results in abnormal microglial response and increased neuron vulnerability to injury. Int J Dev Neurosci 13(3-4):285-99. [PubMed: 7572282]  [MGI Ref ID J:30212]

Bergmann CE; Hoefer IE; Meder B; Roth H; van Royen N; Breit SM; Jost MM; Aharinejad S; Hartmann S; Buschmann IR. 2006. Arteriogenesis depends on circulating monocytes and macrophage accumulation and is severely depressed in op/op mice. J Leukoc Biol 80(1):59-65. [PubMed: 16684892]  [MGI Ref ID J:110465]

Blevins G; Fedoroff S. 1995. Microglia in colony-stimulating factor 1-deficient op/op mice. J Neurosci Res 40(4):535-44. [PubMed: 7616613]  [MGI Ref ID J:23600]

Brown NJ; Hutcheson J; Bickel E; Scatizzi JC; Albee LD; Haines GK rd; Eslick J; Bradley K; Taricone E; Perlman H. 2004. Fas death receptor signaling represses monocyte numbers and macrophage activation in vivo. J Immunol 173(12):7584-93. [PubMed: 15585886]  [MGI Ref ID J:94851]

Bruhns P; Samuelsson A; Pollard JW; Ravetch JV. 2003. Colony-stimulating factor-1-dependent macrophages are responsible for IVIG protection in antibody-induced autoimmune disease. Immunity 18(4):573-81. [PubMed: 12705859]  [MGI Ref ID J:83013]

Carenini S; Maurer M; Werner A; Blazyca H; Toyka KV; Schmid CD; Raivich G; Martini R. 2001. The role of macrophages in demyelinating peripheral nervous system of mice heterozygously deficient in p0. J Cell Biol 152(2):301-8. [PubMed: 11266447]  [MGI Ref ID J:67581]

Cecchini MG; Dominguez MG; Mocci S; Wetterwald A; Felix R; Fleisch H; Chisholm O; Hofstetter W; Pollard JW; Stanley ER. 1994. Role of colony stimulating factor-1 in the establishment and regulation of tissue macrophages during postnatal development of the mouse. Development 120(6):1357-72. [PubMed: 8050349]  [MGI Ref ID J:18915]

Chang MD; Stanley ER; Khalili H; Chisholm O; Pollard JW. 1995. Osteopetrotic (op/op) mice deficient in macrophages have the ability to mount a normal T-cell-dependent immune response. Cell Immunol 162(1):146-52. [PubMed: 7704903]  [MGI Ref ID J:24207]

Chang Y; Albright S; Lee F. 1994. Cytokines in the central nervous system: expression of macrophage colony stimulating factor and its receptor during development. J Neuroimmunol 52(1):9-17. [PubMed: 8207122]  [MGI Ref ID J:19249]

Clohisy DR; Ramnaraine ML. 1997. Osteoclast formation during tumor osteolysis does not require proliferating osteoclast precursor cells. J Orthop Res 15(2):301-6. [PubMed: 9167635]  [MGI Ref ID J:41527]

Clynes R; Ravetch JV. 1995. Cytotoxic antibodies trigger inflammation through Fc receptors. Immunity 3(1):21-6. [PubMed: 7621075]  [MGI Ref ID J:78887]

Cohen PE; Chisholm O; Arceci RJ; Stanley ER; Pollard JW. 1996. Absence of colony-stimulating factor-1 in osteopetrotic (csfmop/csfmop) mice results in male fertility defects. Biol Reprod 55(2):310-7. [PubMed: 8828834]  [MGI Ref ID J:34371]

Cohen PE; Hardy MP; Pollard JW. 1997. Colony-stimulating factor-1 plays a major role in the development of reproductive function in male mice. Mol Endocrinol 11(11):1636-50. [PubMed: 9328346]  [MGI Ref ID J:43181]

Cohen PE; Zhu L; Pollard JW. 1997. Absence of colony stimulating factor-1 in osteopetrotic (csfmop/csfmop) mice disrupts estrous cycles and ovulation. Biol Reprod 56(1):110-8. [PubMed: 9002639]  [MGI Ref ID J:38039]

D'Errico JA; MacNeil RL; Strayhorn CL; Piotrowski BT; Somerman MJ. 1995. Models for the study of cementogenesis. Connect Tissue Res 33(1-3):9-17. [PubMed: 7554968]  [MGI Ref ID J:30202]

Dai XM; Ryan GR; Hapel AJ; Dominguez MG; Russell RG; Kapp S; Sylvestre V; Stanley ER. 2002. Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte deficiency, increased primitive progenitor cell frequencies, and reproductive defects. Blood 99(1):111-20. [PubMed: 11756160]  [MGI Ref ID J:73663]

Dai XM; Zong XH; Sylvestre V; Stanley ER. 2004. Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1-deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1. Blood 103(3):1114-23. [PubMed: 14525772]  [MGI Ref ID J:87641]

De Ciuceis C; Amiri F; Brassard P; Endemann DH; Touyz RM; Schiffrin EL. 2005. Reduced vascular remodeling, endothelial dysfunction, and oxidative stress in resistance arteries of angiotensin II-infused macrophage colony-stimulating factor-deficient mice: evidence for a role in inflammation in angiotensin-induced vascular injury. Arterioscler Thromb Vasc Biol 25(10):2106-13. [PubMed: 16100037]  [MGI Ref ID J:114425]

Deckers MM; Van Beek ER; Van Der Pluijm G; Wetterwald A; Van Der Wee-Pals L; Cecchini MG; Papapoulos SE; Lowik CW. 2002. Dissociation of angiogenesis and osteoclastogenesis during endochondral bone formation in neonatal mice. J Bone Miner Res 17(6):998-1007. [PubMed: 12054176]  [MGI Ref ID J:112373]

Dhawan J; Rando TA; Elson SE; Lee F; Stanley ER; Blau HM. 1996. Myoblast-mediated expression of colony stimulating factor-1 (CSF-1) in the cytokine-deficient op/op mouse. Somat Cell Mol Genet 22(5):363-81. [PubMed: 9039846]  [MGI Ref ID J:38812]

Felix R; Cecchini MG; Fleisch H. 1990. Macrophage colony stimulating factor restores in vivo bone resorption in the op/op osteopetrotic mouse. Endocrinology 127(5):2592-4. [PubMed: 2146111]  [MGI Ref ID J:10799]

Felix R; Hofstetter W; Wetterwald A; Cecchini MG; Fleisch H. 1994. Role of colony-stimulating factor-1 in bone metabolism. J Cell Biochem 55(3):340-9. [PubMed: 7962166]  [MGI Ref ID J:19367]

Feltis BA; Jechorek RP; Erlandsen SL; Wells CL. 1994. Bacterial translocation and lipopolysaccharide-induced mortality in genetically macrophage-deficient op/op mice. Shock 2(1):29-33. [PubMed: 7735981]  [MGI Ref ID J:20379]

Galeazzi F; Lovato P; Blennerhassett PA; Haapala EM; Vallance BA; Collins SM. 2001. Neural change in Trichinella-infected mice is MHC II independent and involves M-CSF-derived macrophages. Am J Physiol Gastrointest Liver Physiol 281(1):G151-8. [PubMed: 11408267]  [MGI Ref ID J:107859]

Ghia JE; Blennerhassett P; El-Sharkawy RT; Collins SM. 2007. The protective effect of the vagus nerve in a murine model of chronic relapsing colitis. Am J Physiol Gastrointest Liver Physiol 293(4):G711-8. [PubMed: 17673544]  [MGI Ref ID J:126720]

Ghia JE; Galeazzi F; Ford DC; Hogaboam CM; Vallance BA; Collins S. 2008. Role of M-CSF-dependent macrophages in colitis is driven by the nature of the inflammatory stimulus. Am J Physiol Gastrointest Liver Physiol 294(3):G770-7. [PubMed: 18202111]  [MGI Ref ID J:132596]

Ginhoux F; Tacke F; Angeli V; Bogunovic M; Loubeau M; Dai XM; Stanley ER; Randolph GJ; Merad M. 2006. Langerhans cells arise from monocytes in vivo. Nat Immunol 7(3):265-73. [PubMed: 16444257]  [MGI Ref ID J:112594]

Gouon-Evans V; Rothenberg ME; Pollard JW. 2000. Postnatal mammary gland development requires macrophages and eosinophils. Development 127(11):2269-82. [PubMed: 10804170]  [MGI Ref ID J:110688]

Guleria I; Pollard JW. 2001. Aberrant macrophage and neutrophil population dynamics and impaired Th1 response to Listeria monocytogenes in colony-stimulating factor 1-deficient mice. Infect Immun 69(3):1795-807. [PubMed: 11179357]  [MGI Ref ID J:67608]

Guleria I; Pollard JW. 2000. The trophoblast is a component of the innate immune system during pregnancy. Nat Med 6(5):589-93. [PubMed: 10802718]  [MGI Ref ID J:119170]

Hume DA; Favot P. 1995. Is the osteopetrotic (op/op mutant) mouse completely deficient in expression of macrophage colony-stimulating factor? J Interferon Cytokine Res 15(4):279-84. [PubMed: 7627801]  [MGI Ref ID J:25708]

Hunt JS; Chen HL; Hu XL; Pollard JW. 1993. Normal distribution of tumor necrosis factor-alpha messenger ribonucleic acid and protein in the uteri, placentas, and embryos of osteopetrotic (op/op) mice lacking colony-stimulating factor-1. Biol Reprod 49(3):441-52. [PubMed: 8399834]  [MGI Ref ID J:14542]

Ida-Yonemochi H; Noda T; Shimokawa H; Saku T. 2002. Disturbed tooth eruption in osteopetrotic (op/op) mice: histopathogenesis of tooth malformation and odontomas. J Oral Pathol Med 31(6):361-73. [PubMed: 12201247]  [MGI Ref ID J:78487]

Ingman WV; Wyckoff J; Gouon-Evans V; Condeelis J; Pollard JW. 2006. Macrophages promote collagen fibrillogenesis around terminal end buds of the developing mammary gland. Dev Dyn 235(12):3222-9. [PubMed: 17029292]  [MGI Ref ID J:116644]

Jang MH; Herber DM; Jiang X; Nandi S; Dai XM; Zeller G; Stanley ER; Kelley VR. 2006. Distinct in vivo roles of colony-stimulating factor-1 isoforms in renal inflammation. J Immunol 177(6):4055-63. [PubMed: 16951369]  [MGI Ref ID J:138044]

Kaku M; Kawata T; Kawasoko S; Fujita T; Tokimasa C; Niida S; Tanne K. 1998. Osteoclast appearance in developmental stages of different bones after a single injection of macrophage colony- stimulating factor in op/op mice. Biomed Res 19(1):77-81.  [MGI Ref ID J:47075]

Kaku M; Kawata T; Kawasoko S; Fujita T; Tokimasa C; Tanne K. 1999. Remodeling of the sagittal suture in osteopetrotic (op/op) mice associated with cranial flat bone growth. J Craniofac Genet Dev Biol 19(2):109-12. [PubMed: 10416154]  [MGI Ref ID J:58056]

Kaku M; Tsutsui K; Motokawa M; Kawata T; Fujita T; Kohno S; Tohma Y; Ohtani J; Tenjoh K; Tanne K. 2003. Amyloid beta protein deposition and neuron loss in osteopetrotic (op/op) mice. Brain Res Brain Res Protoc 12(2):104-8. [PubMed: 14613812]  [MGI Ref ID J:87261]

Kalla R; Liu Z; Xu S; Koppius A; Imai Y; Kloss CU; Kohsaka S; Gschwendtner A; Moller JC; Werner A; Raivich G. 2001. Microglia and the early phase of immune surveillance in the axotomized facial motor nucleus: Impaired microglial activation and lymphocyte recruitment but no effect on neuronal survival or axonal regeneration in macrophage-colony stimulating factor-deficient mice. J Comp Neurol 436(2):182-201. [PubMed: 11438923]  [MGI Ref ID J:70370]

Karlsson MC; Guinamard R; Bolland S; Sankala M; Steinman RM; Ravetch JV. 2003. Macrophages control the retention and trafficking of B lymphocytes in the splenic marginal zone. J Exp Med 198(2):333-40. [PubMed: 12874264]  [MGI Ref ID J:119256]

Kawata T; Fujita T; Tokimasa C; Sugiyama H; Ozawa S; Tanne K. 2001. Analysis of histochemically and morphometrically in the anterior belly digastric muscle of osteopetrotic (op/op) mice. Exp Anim 50(2):133-8. [PubMed: 11381616]  [MGI Ref ID J:69954]

Kawata T; Kawasoko S; Kaku M; Fujita T; Tokimasa C; Niida S ; Tanne K. 1999. Recruitment of osteoclasts in the mandibular condyle of growing osteopetrotic (op/op) mice after a single injection of macrophage colony-stimulating factor. Arch Oral Biol 44(1):81-8. [PubMed: 10075153]  [MGI Ref ID J:53698]

Kawata T; Tokimasa C; Fujita T; Kaku M; Kawasoko S; Sugiyama H ; Ozawa S ; Tanne K. 1999. Morphological change of the nasopremaxillary suture in growing toothless osteopetrotic (op/op) mice. J Craniofac Genet Dev Biol 19(1):48-55. [PubMed: 10378148]  [MGI Ref ID J:55462]

Kawata T; Tokimasa C; Fujita T; Kawasoko S; Kaku M; Sugiyama H; Tanne K. 1998. Midpalatal suture of osteopetrotic (op/op) mice exhibits immature fusion. Exp Anim 47(4):277-81. [PubMed: 10067173]  [MGI Ref ID J:51854]

Kawata T; Tokimasa C; Fujita T; Ozawa S; Sugiyama H; Tanne K. 1999. Facial skeletal growth in growing 'toothless' osteopetrotic (op/op) mice: radiographic findings J Craniofac Genet Dev Biol 19(4):221-5. [PubMed: 10731091]  [MGI Ref ID J:61237]

Kawata T; Tokimasa C; Nowroozi N; Fujita T; Kaku M; Kawasoko S ; Sugiyama H ; Ozawa S ; Zernik JH ; Tanne K. 1999. Lack of the bone remodeling in osteopetrotic (op/op) mice associated with microdontia. J Craniofac Genet Dev Biol 19(2):113-7. [PubMed: 10416155]  [MGI Ref ID J:56255]

Kawata T; Zernik JH; Fujita T; Tokimasa C; Tanne K. 1999. Mechanism in inhibitory effects of vitamin K2 on osteoclastic bone resorption: in vivo study in osteopetrotic (op/op) mice. J Nutr Sci Vitaminol (Tokyo) 45(4):501-7. [PubMed: 10575640]  [MGI Ref ID J:59641]

Kim EY; Battaile JT; Patel AC; You Y; Agapov E; Grayson MH; Benoit LA; Byers DE; Alevy Y; Tucker J; Swanson S; Tidwell R; Tyner JW; Morton JD; Castro M; Polineni D; Patterson GA; Schwendener RA; Allard JD; Peltz G; Holtzman MJ. 2008. Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease. Nat Med 14(6):633-40. [PubMed: 18488036]  [MGI Ref ID J:136947]

Kiso Y; Pollard JW; Croy BA. 1992. A study of granulated metrial gland cell differentiation in pregnant, macrophage-deficient, osteopetrotic (op/op) mice. Experientia 48(10):973-5. [PubMed: 1426147]  [MGI Ref ID J:3619]

Ko EA; Amiri F; Pandey NR; Javeshghani D; Leibovitz E; Touyz RM; Schiffrin EL. 2007. Resistance artery remodeling in deoxycorticosterone acetate-salt hypertension is dependent on vascular inflammation: evidence from m-CSF-deficient mice. Am J Physiol Heart Circ Physiol 292(4):H1789-95. [PubMed: 17142347]  [MGI Ref ID J:125825]

Kobayashi M; Masuda Y; Kishino M; Ishida T; Maeda N; Morimoto T. 2002. Characteristics of mastication in the anodontic mouse. J Dent Res 81(9):594-7. [PubMed: 12202638]  [MGI Ref ID J:105926]

Kodama H; Yamasaki A; Abe M; Niida S; Hakeda Y; Kawashima H. 1993. Transient recruitment of osteoclasts and expression of their function in osteopetrotic (op/op) mice by a single injection of macrophage colony-stimulating factor. J Bone Miner Res 8(1):45-50. [PubMed: 8427048]  [MGI Ref ID J:4732]

Kodama I; Niida S; Sanada M; Yoshiko Y; Tsuda M; Maeda N; Ohama K. 2004. Estrogen regulates the production of VEGF for osteoclast formation and activity in op/op mice. J Bone Miner Res 19(2):200-6. [PubMed: 14969389]  [MGI Ref ID J:111232]

Kondo Y; Lemere CA; Seabrook TJ. 2007. Osteopetrotic (op/op) mice have reduced microglia, no Abeta deposition, and no changes in dopaminergic neurons. J Neuroinflammation 4:31. [PubMed: 18093340]  [MGI Ref ID J:132962]

Lagasse E; Weissman IL. 1997. Enforced expression of Bcl-2 in monocytes rescues macrophages and partially reverses osteopetrosis in op/op mice. Cell 89(7):1021-31. [PubMed: 9215625]  [MGI Ref ID J:41240]

Lane PW. 1973. Osteopetrosis (op) Mouse News Lett 48:35.  [MGI Ref ID J:35678]

Lenda DM; Kikawada E; Stanley ER; Kelley VR. 2003. Reduced macrophage recruitment, proliferation, and activation in colony-stimulating factor-1-deficient mice results in decreased tubular apoptosis during renal inflammation. J Immunol 170(6):3254-62. [PubMed: 12626584]  [MGI Ref ID J:82301]

Lenda DM; Stanley ER; Kelley VR. 2004. Negative role of colony-stimulating factor-1 in macrophage, T cell, and B cell mediated autoimmune disease in MRL-Fas(lpr) mice. J Immunol 173(7):4744-54. [PubMed: 15383612]  [MGI Ref ID J:93714]

Li J; Chen K; Zhu L; Pollard JW. 2006. Conditional deletion of the colony stimulating factor-1 receptor (c-fms proto-oncogene) in mice. Genesis 44(7):328-35. [PubMed: 16823860]  [MGI Ref ID J:110981]

Lieschke GJ; Stanley E; Grail D; Hodgson G; Sinickas V; Gall JA; Sinclair RA; Dunn AR. 1994. Mice lacking both macrophage- and granulocyte-macrophage colony-stimulating factor have macrophages and coexistent osteopetrosis and severe lung disease. Blood 84(1):27-35. [PubMed: 8018921]  [MGI Ref ID J:19089]

Lin EY; Li JF; Bricard G; Wang W; Deng Y; Sellers R; Porcelli SA; Pollard JW. 2007. VEGF Restores Delayed Tumor Progression in Tumors Depleted of Macrophages. Mol Oncol 1(3):288-302. [PubMed: 18509509]  [MGI Ref ID J:138643]

Lin EY; Li JF; Gnatovskiy L; Deng Y; Zhu L; Grzesik DA; Qian H; Xue XN; Pollard JW. 2006. Macrophages regulate the angiogenic switch in a mouse model of breast cancer. Cancer Res 66(23):11238-46. [PubMed: 17114237]  [MGI Ref ID J:116132]

Lin EY; Nguyen AV; Russell RG; Pollard JW. 2001. Colony-stimulating factor 1 promotes progression of mammary tumors to malignancy. J Exp Med 193(6):727-40. [PubMed: 11257139]  [MGI Ref ID J:68146]

Lin EY; Pollard JW. 2004. Macrophages: modulators of breast cancer progression. Novartis Found Symp 256:158-68; discussion 168-72, 259. [PubMed: 15027489]  [MGI Ref ID J:90229]

Lomas-Neira J; Chung CS; Perl M; Gregory S; Biffl W; Ayala A. 2006. Role of alveolar macrophage and migrating neutrophils in hemorrhage-induced priming for ALI subsequent to septic challenge. Am J Physiol Lung Cell Mol Physiol 290(1):L51-8. [PubMed: 16157517]  [MGI Ref ID J:104798]

Lu L; Osmond DG. 2001. Regulation of cell survival during B lymphopoiesis in mouse bone marrow: enhanced pre-B-cell apoptosis in CSF-1-deficient op/op mutant mice. Exp Hematol 29(5):596-601. [PubMed: 11376872]  [MGI Ref ID J:69425]

Mackler AM; Barber EM; Takikawa O; Pollard JW. 2003. Indoleamine 2,3-dioxygenase is regulated by IFN-gamma in the mouse placenta during Listeria monocytogenes infection. J Immunol 170(2):823-30. [PubMed: 12517946]  [MGI Ref ID J:127135]

Maeda N; Kawata T; Yoshiko Y; Hosoi M; Suemune S; Okada N; Tanne K. 1994. Postnatal changes in the masseter muscle of the toothless (op/op) mouse with less-developed periodontal ligaments. Biomed Res 15(4):255-261.  [MGI Ref ID J:20589]

Marks SC Jr; Iizuka T; MacKay CA; Mason-Savas A; Cielinski MJ. 1997. The effects of colony-stimulating factor-1 on the number and ultrastructure of osteoclasts in toothless (tl) rats and osteopetrotic (op) mice. Tissue Cell 29(5):589-95. [PubMed: 9364807]  [MGI Ref ID J:44590]

Marks SC Jr; Lane PW. 1976. Osteopetrosis, a new recessive skeletal mutation on chromosome 12 of the mouse. J Hered 67(1):11-18. [PubMed: 1262696]  [MGI Ref ID J:5634]

McCary LC; DeLuca HF. 1996. Osteopetrotic (op/op) mice are unable to maintain serum calcium levels despite hyperabsorption of calcium. Endocrinology 137(3):1049-56. [PubMed: 8603573]  [MGI Ref ID J:31874]

McCary LC; Smith CM; DeLuca HF. 1997. Hypophosphatemia and the development of rickets in osteopetrotic (op/op) mice. J Bone Miner Res 12(11):1944-51. [PubMed: 9383699]  [MGI Ref ID J:44543]

McCary LC; Staun M; DeLuca HF. 1999. A characterization of vitamin D-independent intestinal calcium absorption in the osteopetrotic (op/op) mouse. Arch Biochem Biophys 368(2):249-56. [PubMed: 10441375]  [MGI Ref ID J:56835]

Menke J; Hsu MY; Byrne KT; Lucas JA; Rabacal WA; Croker BP; Zong XH; Stanley ER; Kelley VR. 2008. Sunlight triggers cutaneous lupus through a CSF-1-dependent mechanism in MRL-Fas(lpr) mice. J Immunol 181(10):7367-79. [PubMed: 18981160]  [MGI Ref ID J:141073]

Michaelson MD; Bieri PL; Mehler MF; Xu H; Arezzo JC; Pollard JW; Kessler JA. 1996. CSF-1 deficiency in mice results in abnormal brain development. Development 122(9):2661-72. [PubMed: 8787741]  [MGI Ref ID J:35818]

Mikkelsen HB; Thuneberg L. 1999. Op/op mice defective in production of functional colony-stimulating factor-1 lack macrophages in muscularis externa of the small intestine. Cell Tissue Res 295(3):485-93. [PubMed: 10022968]  [MGI Ref ID J:53792]

Moayeri M; Martinez NW; Wiggins J; Young HA; Leppla SH. 2004. Mouse susceptibility to anthrax lethal toxin is influenced by genetic factors in addition to those controlling macrophage sensitivity. Infect Immun 72(8):4439-47. [PubMed: 15271901]  [MGI Ref ID J:91775]

Mueller CG; Cremer I; Paulet PE; Niida S; Maeda N; Lebeque S; Fridman WH; Sautes-Fridman C. 2001. Mannose receptor ligand-positive cells express the metalloprotease decysin in the B cell follicle. J Immunol 167(9):5052-60. [PubMed: 11673514]  [MGI Ref ID J:67032]

Mullaly SC; Kubes P. 2006. The role of TLR2 in vivo following challenge with Staphylococcus aureus and prototypic ligands. J Immunol 177(11):8154-63. [PubMed: 17114491]  [MGI Ref ID J:140680]

Murase S; Hayashi Y. 1998. Expression pattern and neurotrophic role of the c-fms proto-oncogene M-CSF receptor in rodent Purkinje cells. J Neurosci 18(24):10481-92. [PubMed: 9852586]  [MGI Ref ID J:52174]

Myint YY; Miyakawa K; Naito M; Shultz LD; Oike Y; Yamamura K; Takahashi K. 1999. Granulocyte/macrophage colony-stimulating factor and interleukin-3 correct osteopetrosis in mice with osteopetrosis mutation. Am J Pathol 154(2):553-66. [PubMed: 10027413]  [MGI Ref ID J:52817]

Nagahama SI; Cunningham ML; Lee MY; Byers MR. 1998. Normal development of dental innervation and nerve/tissue interactions in the colony-stimulating factor-1 deficient osteopetrotic mouse. Dev Dyn 211(1):52-9. [PubMed: 9438423]  [MGI Ref ID J:45196]

Naito M; Hayashi S; Yoshida H; Nishikawa S; Shultz LD; Takahashi K. 1991. Abnormal differentiation of tissue macrophage populations in 'osteopetrosis' (op) mice defective in the production of macrophage colony-stimulating factor. Am J Pathol 139(3):657-67. [PubMed: 1887865]  [MGI Ref ID J:26978]

Naito M; Umeda S; Takahashi K; Shultz LD. 1997. Macrophage differentiation and granulomatous inflammation in osteopetrotic mice (op/op) defective in the production of CSF-1. Mol Reprod Dev 46(1):85-91. [PubMed: 8981368]  [MGI Ref ID J:37427]

Nandi S; Akhter MP; Seifert MF; Dai XM; Stanley ER. 2006. Developmental and functional significance of the CSF-1 proteoglycan chondroitin sulfate chain. Blood 107(2):786-95. [PubMed: 16210339]  [MGI Ref ID J:126635]

Neugarten J; Feith GW; Assmann KJ; Shan Z; Stanley ER; Schlondorff D. 1995. Role of macrophages and colony-stimulating factor-1 in murine antiglomerular basement membrane glomerulonephritis. J Am Soc Nephrol 5(11):1903-9. [PubMed: 7542490]  [MGI Ref ID J:26586]

Ngo VN; Korner H; Gunn MD; Schmidt KN; Riminton DS; Cooper MD; Browning JL; Sedgwick JD; Cyster JG. 1999. Lymphotoxin alpha/beta and tumor necrosis factor are required for stromal cell expression of homing chemokines in B and T cell areas of the spleen. J Exp Med 189(2):403-12. [PubMed: 9892622]  [MGI Ref ID J:52941]

Niida S; Abe M; Suemune S; Yoshiko Y; Maeda N; Yamasaki A. 1997. Restoration of disturbed tooth eruption in osteopetrotic (op/op) mice by injection of macrophage colony-stimulating factor. Exp Anim 46(2):95-101. [PubMed: 9145288]  [MGI Ref ID J:40564]

Niida S; Kondo T; Hiratsuka S; Hayashi S; Amizuka N; Noda T; Ikeda K; Shibuya M. 2005. VEGF receptor 1 signaling is essential for osteoclast development and bone marrow formation in colony-stimulating factor 1-deficient mice. Proc Natl Acad Sci U S A 102(39):14016-21. [PubMed: 16172397]  [MGI Ref ID J:101408]

Niida S; Wakisaka H; Kanno E; Yamasaki A. 1994. Cranial flat bone formation in the osteopetrotic (Op/Op) mouse Biomed Res 15(1):37-44.  [MGI Ref ID J:18356]

Nilsson SK; Bertoncello I. 1994. Age-related changes in extramedullary hematopoiesis in the spleen of normal and perturbed osteopetrotic (op/op) mice [published erratum appears in Exp Hematol 1994 Jun;22(6):527-8] Exp Hematol 22(4):377-83. [PubMed: 8150037]  [MGI Ref ID J:17699]

Nilsson SK; Bertoncello I. 1994. The development and establishment of hemopoiesis in fetal and newborn osteopetrotic (op/op) mice. Dev Biol 164(2):456-62. [PubMed: 8045348]  [MGI Ref ID J:19549]

Nilsson SK; Lieschke GJ; Garcia-Wijnen CC; Williams B; Tzelepis D; Hodgson G; Grail D; Dunn AR; Bertoncello I. 1995. Granulocyte-macrophage colony-stimulating factor is not responsible for the correction of hematopoietic deficiencies in the maturing op/op mouse. Blood 86(1):66-72. [PubMed: 7795257]  [MGI Ref ID J:26516]

Nishino I; Amizuka N; Ozawa H. 2001. Histochemical examination of osteoblastic activity in op/op mice with or without injection of recombinant M-CSF. J Bone Miner Metab 19(5):267-76. [PubMed: 11498728]  [MGI Ref ID J:117405]

Nishioji K; Okanoue T; Mori T; Sakamoto S; Itoh Y. 1999. Experimental liver injury induced by Propionibacterium acnes and lipopolysaccharide in macrophage colony stimulating factor-deficient osteopetrotic (op/op) mice. Dig Dis Sci 44(10):1975-84. [PubMed: 10548345]  [MGI Ref ID J:59689]

Nowicki A; Szenajch J; Ostrowska G; Wojtowicz A; Wojtowicz K; Kruszewski AA; Maruszynski M; Aukerman SL; Wiktor-Jedrzejczak W. 1996. Impaired tumor growth in colony-stimulating factor 1 (CSF-1)-deficient, macrophage-deficient op/op mouse: evidence for a role of CSF-1-dependent macrophages in formation of tumor stroma. Int J Cancer 65(1):112-9. [PubMed: 8543387]  [MGI Ref ID J:31373]

Oguma K; Oshima H; Aoki M; Uchio R; Naka K; Nakamura S; Hirao A; Saya H; Taketo MM; Oshima M. 2008. Activated macrophages promote Wnt signalling through tumour necrosis factor-alpha in gastric tumour cells. EMBO J 27(12):1671-81. [PubMed: 18511911]  [MGI Ref ID J:137013]

Ovadia S; Insogna K; Yao GQ. 2006. The cell-surface isoform of colony stimulating factor 1 (CSF1) restores but does not completely normalize fecundity in CSF1-deficient mice. Biol Reprod 74(2):331-6. [PubMed: 16237150]  [MGI Ref ID J:105388]

Owens GC; Bunge RP. 1991. Schwann cells infected with a recombinant retrovirus expressing myelin-associated glycoprotein antisense RNA do not form myelin. Neuron 7(4):565-75. [PubMed: 1718333]  [MGI Ref ID J:26987]

Pasparakis M; Kousteni S; Peschon J; Kollias G. 2000. Tumor necrosis factor and the p55TNF receptor are required for optimal development of the marginal sinus and for migration of follicular dendritic cell precursors into splenic follicles. Cell Immunol 201(1):33-41. [PubMed: 10805971]  [MGI Ref ID J:62236]

Philippart C; Tzehoval E; Moricard Y; Bringuier AF; Seebold C; Lemoine FM; Arys A; Dourov N; Labat ML. 1993. Immune cell defects affect bone remodelling in osteopetrotic op/op mice. Bone Miner 23(3):317-32. [PubMed: 8148672]  [MGI Ref ID J:18531]

Pollard JW; Dominguez MG; Mocci S; Cohen PE; Stanley ER. 1997. Effect of the colony-stimulating factor-1 null mutation, osteopetrotic (csfm(op)), on the distribution of macrophages in the male mouse reproductive tract. Biol Reprod 56(5):1290-300. [PubMed: 9160730]  [MGI Ref ID J:40266]

Pollard JW; Hennighausen L. 1994. Colony stimulating factor 1 is required for mammary gland development during pregnancy. Proc Natl Acad Sci U S A 91(20):9312-6. [PubMed: 7937762]  [MGI Ref ID J:20519]

Pollard JW; Hunt JS; Wiktor-Jedrzejczak W; Stanley ER. 1991. A pregnancy defect in the osteopetrotic (op/op) mouse demonstrates the requirement for CSF-1 in female fertility. Dev Biol 148(1):273-83. [PubMed: 1834496]  [MGI Ref ID J:70400]

Pull SL; Doherty JM; Mills JC; Gordon JI; Stappenbeck TS. 2005. Activated macrophages are an adaptive element of the colonic epithelial progenitor niche necessary for regenerative responses to injury. Proc Natl Acad Sci U S A 102(1):99-104. [PubMed: 15615857]  [MGI Ref ID J:95824]

Qiao JH; Tripathi J; Mishra NK; Cai Y; Tripathi S; Wang XP; Imes S ; Fishbein MC ; Clinton SK ; Libby P ; Lusis AJ ; Rajavashisth TB. 1997. Role of macrophage colony-stimulating factor in atherosclerosis: studies of osteopetrotic mice. Am J Pathol 150(5):1687-99. [PubMed: 9137093]  [MGI Ref ID J:40136]

Raivich G; Moreno-Flores MT; Moller JC; Kreutzberg GW. 1994. Inhibition of posttraumatic microglial proliferation in a genetic model of macrophage colony-stimulating factor deficiency in the mouse. Eur J Neurosci 6(10):1615-8. [PubMed: 7850025]  [MGI Ref ID J:128182]

Rajavashisth T; Qiao JH; Tripathi S; Tripathi J; Mishra N; Hua M ; Wang XP ; Loussararian A ; Clinton S ; Libby P ; Lusis A. 1998. Heterozygous osteopetrotic (op) mutation reduces atherosclerosis in LDL receptor- deficient mice. J Clin Invest 101(12):2702-10. [PubMed: 9637704]  [MGI Ref ID J:48300]

Ryan GR; Dai XM; Dominguez MG; Tong W; Chuan F; Chisholm O; Russell RG; Pollard JW; Stanley ER. 2001. Rescue of the colony-stimulating factor 1 (CSF-1)-nullizygous mouse (Csf1(op)/Csf1(op)) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis. Blood 98(1):74-84. [PubMed: 11418465]  [MGI Ref ID J:70188]

Sasaki A; Yokoo H; Naito M; Kaizu C; Shultz LD; Nakazato Y. 2000. Effects of macrophage-colony-stimulating factor deficiency on the maturation of microglia and brain macrophages and on their expression of scavenger receptor. Neuropathology 20(2):134-42. [PubMed: 10935450]  [MGI Ref ID J:82594]

Schonlau F; Schlesiger C; Ehrchen J; Grabbe S; Sorg C; Sunderkotter C. 2003. Monocyte and macrophage functions in M-CSF-deficient op/op mice during experimental leishmaniasis. J Leukoc Biol 73(5):564-73. [PubMed: 12714570]  [MGI Ref ID J:120654]

Shibata Y; Zsengeller Z; Otake K; Palaniyar N; Trapnell BC. 2001. Alveolar macrophage deficiency in osteopetrotic mice deficient in macrophage colony-stimulating factor is spontaneously corrected with age and associated with matrix metalloproteinase expression and emphysema. Blood 98(9):2845-52. [PubMed: 11675359]  [MGI Ref ID J:72385]

Smith JD; Trogan E; Ginsberg M; Grigaux C; Tian J; Miyata M. 1995. Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor (op) and apolipoprotein E. Proc Natl Acad Sci U S A 92(18):8264-8. [PubMed: