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Low blood fluid shear stress (SS) promotes vascular remodeling and atherosclerosis; however, the effects of high (H)SS on vascular remodeling and atherogenesis is not fully clarified. The major goal of this study was to investigate the role of HSS in atherosclerotic plaque formation. A perivascular SS modifier was implanted in the right carotid artery of apolipoprotein E (ApoE) ‑/‑ mice to induce HSS, whereas the left carotid artery represented undisturbed (U)SS as a control in vivo . In vitro modeling used human umbilical vein endothelial cells and vascular smooth muscle cells exposed to HSS (2.5 Pa) using a parallel‑plate flow system. The results demonstrated that there were no plaque formations or endothelial cells in the HSS regions of the carotid artery in ApoE ‑/‑ mice. The number of umbilical vein endothelial cells was markedly decreased in a time‑dependent manner in HSS. HSS significantly decreased α‑smooth muscle actin and increased osteopontin protein expression levels compared with USS in vascular smooth muscle cells (P&lt;0.05). In addition, HSS significantly increased the protein expression levels of collagen α1(XVIII) chain/endostatin and matrix metalloproteinase‑8 in vascular smooth muscle cells. These data indicated that HSS may prevent atherosclerotic plaque formation through endothelium denudation and contractile‑to‑synthetic phenotypic conversion of smooth muscle cells.

molecular medicine reports

High fluid shear stress prevents atherosclerotic plaque formation by promoting endothelium denudation and synthetic phenotype of vascular smooth muscle cells