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PLGF expression in coronary artery smooth muscle cells is sensitive to changes in shear stress

Hemodynamic forces (stretch and shear stress) have a profound effect on the vasculature by regulating collateral artery remodeling (arteriogenesis) and development of atherosclerotic plaque. Placental growth factor (PLGF) stimulates arteriogenesis via monocyte recruitment. However, little is known about the effects of hemodynamic forces on PLGF. Based on a previous finding that arterial ligation increases PLGF in downstream collaterals, we hypothesized that PLGF is regulated by shear stress. To test this hypothesis, human coronary artery smooth muscle cells (HCASMC) were grown on the bottom of porous inserts and human coronary endothelial cells (HCAEC) were grown on the top. The HCAEC layer was then exposed to 3 levels of shear for 2 h in a cone and plate device (time‐averaged shear of 10 dyn/cm2 mimicking normal coronary artery flow; 2.5 dyn/cm2recirculatory shear simulating turbulent flow post‐stenosis; or no shear) (N=5 experiments in duplicate). Shear did not affect PLGF mRNA in HCAEC (qPCR). Interestingly, however, PLGF mRNA in HCASMC was increased by ~50% by normal shear, compared to recirculatory shear (p<0.05), although HCASMC were not directly exposed to shear. Preliminary PLGF protein analysis (ELISA) was consistent with the RNA data. These findings suggest that PLGF expression in HCASMC may be regulated by hemodynamic forces in an endothelium‐dependent manner. Funding: NIH R01 HL084494 (PL).