MCSF expression is induced in healing XXXX and may regulate monocyte and endothelial cell phenotype.

@entity63 @entity235 @entity2306 @entity11615 @entity1188 @entity14119 @entity1562 @entity583 @entity4149 @entity4357
@entity583 is associated with the rapid induction of mononuclear cell chemoattractants that promote monocyte infiltration into the injured area. Monocyte-to-macrophage differentiation and macrophage proliferation allow a long survival of monocytic cells, critical for effective healing of the @entity1188 . In a @entity235 @entity1188 -reperfusion model, newly recruited myeloid leukocytes were markedly augmented during early reperfusion (5-72 h). By 7 days, the number of newly recruited myeloid cells was reduced, and the majority of the inflammatory cells remaining in the @entity1188 were mature macrophages. Macrophage colony-stimulating factor (MCSF) is known to facilitate monocyte survival, monocyte-to-macrophage conversion, and macrophage proliferation. We demonstrated marked induction of MCSF mRNA in @entity63 segments persisting for at least 5 days after reperfusion. MCSF expression was predominantly localized to mature macrophages infiltrating the infarcted @entity1562 ; the expression of the MCSF receptor, c-Fms, a protein with @entity4149 kinase activity, was found in these macrophages but was also observed in a subset of microvessels within the @entity1188 . Many @entity1188 macrophages expressed proliferating cell nuclear antigen, a marker of proliferative activity. In vitro MCSF induced @entity14119 synthesis in @entity235 venous endothelial cells. MCSF-induced endothelial @entity14119 upregulation was inhibited by @entity11615 , a @entity4149 kinase inhibitor, and by @entity2306 , a @entity4357 3'-kinase inhibitor. We suggest that upregulation of MCSF in the infarcted @entity1562 may have an active role in healing not only through its effects on cells of monocyte/macrophage lineage, but also by regulating endothelial cell chemokine expression.
