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eNOS-NO-induced small blood vessel relaxation requires EHD2-dependent caveolae stabilization

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Item Type:Article
Title:eNOS-NO-induced small blood vessel relaxation requires EHD2-dependent caveolae stabilization
Creators Name:Matthaeus, C. and Lian, X. and Kunz, S. and Lehmann, M. and Zhong, C. and Bernert, C. and Lahmann, I. and Müller, D.N. and Gollasch, M. and Daumke, O.
Abstract:Endothelial nitric oxide synthase (eNOS)-related vessel relaxation is a highly coordinated process that regulates blood flow and pressure and is dependent on caveolae. Here, we investigated the role of caveolar plasma membrane stabilization by the dynamin-related ATPase EHD2 on eNOS-nitric oxide (NO)-dependent vessel relaxation. Loss of EHD2 in small arteries led to increased numbers of caveolae that were detached from the plasma membrane. Concomitantly, impaired relaxation of mesenteric arteries and reduced running wheel activity were observed in EHD2 knockout mice. EHD2 deletion or knockdown led to decreased production of nitric oxide (NO) although eNOS expression levels were not changed. Super-resolution imaging revealed that eNOS was redistributed from the plasma membrane to internalized detached caveolae in EHD2-lacking tissue or cells. Following an ATP stimulus, reduced cytosolic Ca(2+) peaks were recorded in human umbilical vein endothelial cells (HUVECs) lacking EHD2. Our data suggest that EHD2-controlled caveolar dynamics orchestrates the activity and regulation of eNOS/NO and Ca(2+) channel localization at the plasma membrane.
Keywords:Animal Physical Conditioning, Blood Vessels, Calcium, Carrier Proteins, Caveolae, Cell Membrane, Cytosol, Human Umbilical Vein Endothelial Cells, Inbred C57BL Mice, Mesenteric Arteries, Nitric Oxide, Nitric Oxide Synthase Type III, Vasodilation, Animals, Mice
Source:PLoS ONE
Publisher:Public Library of Science
Page Range:e0223620
Date:10 October 2019
Official Publication:https://doi.org/10.1371/journal.pone.0223620
PubMed:View item in PubMed

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