PDF(Pubmed)
Abstract：
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<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.
摘要：
低血液流体剪切应力（SS）促进血管重塑和动脉粥样硬化；然而，高（H）SS对血管重塑和动脉粥样硬化的影响尚未完全阐明。本研究的主要目的是研究HSS在动脉粥样硬化斑块形成中的作用。将血管周围SS修饰剂植入载脂蛋白E（ApoE）-/小鼠的右颈动脉中以诱导HSS，而左颈动脉代表无干扰（U）SS作为体内对照。体外建模使用人脐静脉内皮细胞和使用平行板流动系统暴露于HSS（2.5Pa）的血管平滑肌细胞。结果表明，ApoE-/-小鼠的颈动脉HSS区域没有斑块形成或内皮细胞。在HSS中，脐静脉内皮细胞的数量以时间依赖性方式显着减少。与USS相比，HSS显著降低了血管平滑肌细胞中α-平滑肌肌动蛋白和骨桥蛋白的表达水平（P<0.05）。此外,HSS显着增加了血管平滑肌细胞中胶原蛋白α1（XVIII）链/内皮抑素和基质金属蛋白酶-8的蛋白质表达水平。这些数据表明，HSS可能通过内皮剥脱和平滑肌细胞的收缩至合成表型转化来预防动脉粥样硬化斑块的形成。
