Characterization of M-CSF and its receptor in microphthalmic mice.
The macrophage colony-stimulating factor (M-CSF) gene expression in osteopetrotic mice (op/op) is defective due to a point-mutation in the M-CSF gene [1]. However, almost all osteopetrotic patients have been shown to have a normal or elevated circulating level of bioactive M-CSF [2]. To investigate the action of the M-CSF in mi/mi mice (microphthalmic; another osteopetrotic mouse mutant), M-CSF levels and its receptors were studied. We found that serum levels of M-CSF in mi/mi mice were not significantly different from normal control mice. The M-CSF receptor binding affinity of spleen-adherent cells was similar to that of control mice. In spleen cells from mi/mi mice, the receptor binding sites per cell (normalized to total spleen cells, M-CSF receptor positive cells, or M-CSF receptor RNA positive cells) were present in a greater number than in spleen cells from phenotypically normal siblings. Northern blot analysis showed that there is no significant difference in transcripts of the M-CSF receptor (c-fms) in the mi/mi and phenotypically normal mice. Unlike the op/op mutant, M-CSF levels, as well as the affinity and number of M-CSF receptors, do not explain the defect in osteoclastic function in the mi/mi mutation.
Yang
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Department of Pediatrics, Medical University of South Carolina, Charleston.
Zhang
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Ries
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D000818:Animals; D015152:Blotting, Northern; D017403:In Situ Hybridization; D016173:Macrophage Colony-Stimulating Factor / Q000097:blood / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains / Q000378:metabolism*; D008850:Microphthalmos / Q000235:genetics / Q000378:metabolism; D010022:Osteopetrosis / Q000235:genetics / Q000378:metabolism*; D011869:Radioligand Assay; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000378:metabolism*; D013154:Spleen / Q000378:metabolism
D016173:Macrophage Colony-Stimulating Factor; D016186:Receptor, Macrophage Colony-Stimulating Factor