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Evidence for a role of endothelial‐cell derived PLGF in paracrine communication

Placenta growth factor (PLGF) is a vascular endothelial growth factor (VEGF)‐family protein that mediates arteriogenesis (adaptive collateral artery remodeling) via a monocyte‐dependent mechanism. In a previous study of 10 different endothelial cell (EC) and vascular smooth muscle cell (SMC) lines, we found that EC express much higher levels of PLGF mRNA and protein than do SMC. The high level of PLGF expression by EC was surprising, as the related factor VEGF is expressed mainly in tissue surrounding EC, rather than in EC. PLGF has been shown not to be mitogenic for EC. Therefore, we hypothesized that the high level of PLGF expression in EC might be important for supporting other EC functions, such as survival, migration, and tube formation. To test this hypothesis, we knocked down PLGF expression in human coronary artery endothelial cells (HCAEC) using siRNA and performed functional assays. Knockdown of PLGF did not affect EC viability. Migration of EC towards VEGF and tube formation in GelTrex were likewise unaffected by PLGF knockdown. Survival of human coronary artery smooth muscle cells (HCASMC) was also unaffected by PLGF siRNA treatment. These results suggest that the high expression of PLGF by EC likely mediates paracrine communication between EC and non‐vascular cells, such as circulating monocytes. Further studies are needed to characterize the secretion of PLGF by EC. Funding: NIH R01 HL084494 (PL).