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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Cells, Cultured, Gene Expression Regulation, Enzymologic, Human Umbilical Vein Endothelial Cells, Humans, Mechanotransduction, Cellular, Nitric Oxide Synthase Type III, RNA Interference, Scavenger Receptors, Class B, Stress, Mechanical, Time Factors, Transfection.
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Does shear stress regulate endothelial cell function through SRB1-eNOS signaling pathway? Context: The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR-B1 signaling transduction. Parallel-plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear stress upon human umbilical vein endothelial cells (HUVECs). The expression of SR-B1 and eNOS at both RNA and protein levels was detected under different dynamic conditions. RNA interference and gene transfection were performed to overexpress and knock down the SRB1 to confirm the role of SR-B1-eNOS signaling pathway. The expression levels of SR-B1 and eNOS were downregulated when HUVECs were treated with 4.2 dyne/cm(2) shear stress compared with those of the control group. However, the expression of SR-B1 and eNOS was upregulated as HUVECs exposed to 8.4 and 15 dyne/cm(2) shear stress. When exposed to 8.4 dyne/cm(2) , SR-B1 and eNOS expression was significantly higher compared with those of the other groups. When SR-B1 was knocked down through RNAi technique, the expression of eNOS was significantly downregulated than those of the other groups. While overexpression of SR-B1 could upregulate eNOS significantly.
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Shear stress regulates endothelial cell function through SR-B1-eNOS signaling pathway. SR-B1 may play a pivotal role in the process of anti-atherosclerosis. Final Decision: yes