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Rapid publication: Impairment of macrophage colony‐stimulating factor production and lack of resident bone marrow macrophages in the osteopetrotic op/op Mouse
Author(s) -
Felix R.,
Cecchini M.G.,
Hofstetter W.,
Elford P.R.,
Stutzer A.,
Fleisch H.
Publication year - 1990
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650050716
Subject(s) - calvaria , macrophage colony stimulating factor , bone resorption , osteoclast , bone marrow , macrophage , resorption , colony stimulating factor , endocrinology , medicine , osteopetrosis , biology , pathology , chemistry , in vitro , stem cell , haematopoiesis , microbiology and biotechnology , biochemistry , receptor
Mouse calvaria‐derived osteoblastlike cells have been shown to produce macrophage colony‐stimulating factor (M‐CSF). This factor may be involved in osteoclastogenesis and thus in bone resorption. In the present study we investigated whether the production of M‐CSF was altered in the osteopetrotic mouse mutant strain op/op , characterized by a decrease in osteoclast number and an impairment of bone resorption. Whole calvariae and cells, as well as skin and lung fibroblasts, of the op/op mouse were found to produce no measurable M‐CSF, in contrast to tissue and cells derived from normal littermates. M‐CSF was identified by colony assay in semisolid media and by inhibition of the biologic activity with antiserum against M‐CSF. Furthermore, the number of resident macrophages, identified by F4/80 antigen (F4/80 Ag) immunohistochemistry, was drastically decreased in bone and bone marrow of the op/op mouse, but in skin these cells were normal in number and morphology. These findings suggest that both M‐CSF and resident macrophages play a role in the mechanism of bone resorption. The op/op mouse appears to be a valuable model to further investigate such a hypothesis.