Molecular mechanism of Flt-1 protein and the regulation of monocytes modulate endothelial cell in wound healing sites via PGF/FLT1 signaling☆

The purpose of this study was to investigate the mechanism of action of the Flt-1 protein molecule during wound healing and to analyze how monocytes regulate endothelial cells at the wound healing site through the placental growth factor/Fms-like tyrosine kinase 1 (PGF/FLT1) signaling pathway. In this study, the PGF and Flt-1 knockdown mice models were constructed to observe the changes of wound healing. The expression of Flt-1 mRNA and protein during wound healing in human and mice biopsies was detected by qPCR and immunofluorescence. The interaction between monocytes and endothelial cells, especially the role of proteins and RNAs in the PGF/FLT1 signaling pathway in this process, was also analyzed. The results showed that the expression of Flt1 protein was significantly up-regulated during wound healing, especially in endothelial cells, which promotes the proliferation and migration of endothelial cells, accelerates angiogenesis, and thus accelerates the rate of wound healing. In contrast, Flt-1 knockdown suppresses these processes. Monocytes can activate the FLT1 receptor on endothelial cells by secreting PGF, and then promote the proliferation and migration of endothelial cells.