Oscillatory shear stress upregulation of endothelial nitric oxide synthase requires intracellular hydrogen peroxide and CaMKII

Journal of Molecular and Cellular Cardiology
Hua CaiDavid G Harrison

Abstract

We have previously shown that hydrogen peroxide (H(2)O(2)) upregulates endothelial nitric oxide synthase (eNOS) expression via a calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated mechanism whereas it also acutely activates eNOS enzyme. We hypothesized that oscillatory shear stress (OSS), which stimulates endogenous H(2)O(2), would have effects on eNOS expression and function similar to that of exogenous H(2)O(2). Exposure of bovine aortic endothelial cells to OSS (+/-15 dynes/cm(2)) increased eNOS mRNA expression by 3-fold. Pretreatment with either polyethylene glycol-catalase (PEG-CAT, a scavenger of H(2)O(2)) or KN93, an inhibitor of CaMKII, abolished this response. OSS activated CaMKII in an H(2)O(2)-dependent fashion whereas unidirectional laminar shear stress (LSS) inhibited CaMKII phosphorylation. Inhibition of c-Src (essential for LSS upregulation of eNOS) had no effect on OSS upregulation of eNOS. Additionally, OSS stimulated NO* production acutely. Scavenging of H(2)O(2) by PEG-CAT attenuated OSS stimulation of NO* by 50% whereas it had no effect on LSS regulation of NO* production. These data suggest that intracellular H(2)O(2) and CaMKII mediate OSS upregulation of eNOS. The acute activation of eNOS by...Continue Reading

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Citations

Jun 9, 2005·Proceedings of the National Academy of Sciences of the United States of America·Karel Chalupsky, Hua Cai
Jan 24, 2007·Physiological Reviews·Pál PacherLucas Liaudet
Jul 10, 2009·Cardiovascular Research·Eric Thorin, Nathalie Thorin-Trescases
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Aug 29, 2020·American Journal of Physiology. Heart and Circulatory Physiology·Cristine L HeapsJanet L Parker

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