Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway

Journal of Cellular Physiology
Yuelin ChaoShao-Liang Chen

Abstract

Reactive oxygen species (ROS) contribute to many aspects of physiological and pathological cardiovascular processes. However, the underlying mechanism of ROS induction by low shear stress (LSS) remains unclear. Accumulating evidence has shown that the angiotensin II type 1 receptor (AT1R) is involved in inflammation, apoptosis, and ROS production. Our aim was to explore the role of AT1R in LSS-mediated ROS induction. We exposed human umbilical vein endothelial cells (HUVECs) to LSS (3 dyn/cm(2) ) for different periods of time. Western blotting and immunofluorescence showed that LSS significantly induced AT1R expression in a time-dependent manner. Using immunohistochemistry, we also noted a similar increase in AT1R expression in the inner curvature of the aortic arch compared to the descending aorta in C57BL/6 mice. Additionally, HUVECs were cultured with a fluorescent probe, either DCFH, DHE or DAF, after being subjected to LSS. Cell chemiluminescence and flow cytometry results revealed that LSS stimulated ROS levels and suppressed nitric oxide (NO) generation in a time-dependent manner, which was reversed by the AT1R antagonist Losartan. We also found that Losartan markedly increased endothelial NO synthase (eNOS) phosphorylat...Continue Reading

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Citations

Dec 12, 2017·Cardiovascular Research·Santa MundiRaffaele De Caterina
Jan 10, 2019·Antioxidants & Redox Signaling·Evgeny A ZemskovStephen M Black
Mar 13, 2019·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Junjie ZhangShaoliang Chen
Nov 14, 2019·Cellular and Molecular Bioengineering·Yan-Xia WangKai-Rong Qin
Oct 16, 2019·Biointerphases·Sudipto DattaPallab Datta
Sep 3, 2019·Journal of Physical Activity & Health·Ryan S GartenJennifer Weggen

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