M-CSF stimulates lipoprotein lipase secretion and mRNA expression in specific macrophage populations, suggesting a role in macrophage lipoprotein metabolism.
Provides mechanistic insight into macrophage LPL regulation; leaves open translational relevance to human atherosclerosis.
The effects of human recombinant macrophage colony-stimulating factor (M-CSF) on the secretion of lipoprotein lipase were studied in rat alveolar macrophages. Five nanograms per milliliter M-CSF significantly enhanced lipoprotein lipase secretion (threefold), and the maximal effect (10-fold) of M-CSF on lipoprotein lipase secretion was observed at a dose of 200 ng/ml M-CSF. The effect of M-CSF was time dependent but was not manifested during the first 8 hours of incubation. After 24 hours, its effects were evident and dose dependent. On blot hybridization of macrophage RNAs with human cDNA of lipoprotein lipase, a remarkable and dose-dependent increase in mRNA level (7.3-fold) was found in M-CSF-treated alveolar macrophages. The secretion of lipoprotein lipase was also enhanced in human monocyte-derived macrophages (2.6-fold), whereas the secretion from either THP-1 cells, P388 cells, or J774 cells was not significantly enhanced. These results indicate that the stimulation of lipoprotein lipase secretion after M-CSF treatment was evident in rat alveolar macrophages and human monocyte-derived macrophages on the basis of both enzyme activity and mRNA level; therefore, M-CSF may be involved in lipoprotein metabolism of macrophages through modulation of the secretion of lipoprotein lipase.
No takes yet. Share an insight, caveat, or question.
Mori et al. (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: