Open AccessJournal Article
Abnormal differentiation of tissue macrophage populations in 'osteopetrosis' (op) mice defective in the production of macrophage colony-stimulating factor.
Makoto Naito,Shin-Ichi Hayashi,Hisahiro Yoshida,Satomi Nishikawa,Leonard D. Shultz,Kiyoshi Takahashi +5 more
TLDR
In co-cultures of normal mouse bone marrow cells with fibroblast cell lines prepared from the lungs of the op/op mice, a defective differentiation of monocytes into macrophages was confirmed, supporting previous evidence that the fibro Blast cell lines of the mutant mouse failed to produce functional macrophage colony-stimulating factor (M-CSF/CSF-1).Abstract:
Examination of the op/op mouse disclosed marked reduction and abnormal differentiation of osteoclasts in the bones and of tissue-specific macrophages in various visceral organs and tissues. Most of these macrophages were immature as judged by ultrastructural criteria. In co-cultures of normal mouse bone marrow cells with fibroblast cell lines prepared from the lungs of the op/op mice, a defective differentiation of monocytes into macrophages was confirmed, supporting previous evidence that the fibroblast cell lines of the mutant mouse failed to produce functional macrophage colony-stimulating factor (M-CSF/CSF-1). In such co-cultures, however, a small number of macrophages apparently mature under the influence of granulocyte/macrophage colony-stimulating factor (GM-CSF) produced by the op/op fibroblast cell lines. In the mutant mice, the numbers of macrophages in the uterine wall and ovaries were severely reduced. Compared with the tissues of normal littermates, those of the mutants contained about 60% fewer macrophages in many tissues. This suggests that an M-CSF-independent population of macrophages is derived from granulocyte/macrophage-colony-forming cells (GM-CFC) or earlier hematopoietic progenitors.read more
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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.
Xuming Dai,Gregory R. Ryan,Andrew J. Hapel,Melissa G. Dominguez,Robert G. Russell,Sara Kapp,Vonetta Sylvestre,E. Richard Stanley +7 more
TL;DR: The results indicate that all of the effects of CSF-1 are mediated via the CSf-1R, but that subtle effects of the CS fms proto-oncogene could result from its CS F-1-independent activation.
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Cytokines and CNS development.
TL;DR: The extensive and diverse requirements for properly regulated cytokine signaling during normal nervous system development revealed by these studies sets the foundation for ongoing and future work aimed at understanding how cytokines induced normally and pathologically during critical stages of fetal development alter nervous system function and behavior later in life.
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Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor (op) and apolipoprotein E
TL;DR: The hypothesis that Macrophage colony-stimulating factor and its effects on macrophage development and function play a key role in atherogenesis is supported.
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Role of colony stimulating factor-1 in the establishment and regulation of tissue macrophages during postnatal development of the mouse
Marco G. Cecchini,M.G. Dominguez,S. Mocci,Antoinette Wetterwald,Rolf Felix,Herbert Fleisch,Orin Chisholm,Willy Hofstetter,J.W. Pollard,E.R. Stanley +9 more
TL;DR: The studies suggest that circulating CSF-1 exclusively regulates both the F4/80+ cells in the liver, spleen and kidney and the MOMA-1+ metallophilic macrophages in the spleen.
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Postnatal mammary gland development requires macrophages and eosinophils.
TL;DR: The data show that CSF1-regulated macrophages, in collaboration with eotaxin-regulated eosinophils, have essential and complementary functions in regulating the branching morphogenesis of the mammary gland.