<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sharma P</submitter><funding>American Heart Association</funding><funding>U.S. Department of Health &amp;amp;amp; Human Services | National Institutes of Health</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | National Institutes of Health (NIH)</funding><funding>American Heart Association (American Heart Association, Inc.)</funding><pagination>14110</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6148090</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>Vascular dysfunction and insulin resistance (IR) are associated with obstructive sleep apnea (OSA), which is characterized by frequent episodes of nocturnal intermittent hypoxia (IH). While it is recognized that the balance between vasoconstrictive (endothelin-1) and vasodilatory molecules (nitric oxide, NO) determine vascular profile, molecular mechanisms contributing to vascular dysfunction and IR in OSA are not completely understood. Caveolin-1 is a membrane protein which regulates endothelial nitric oxide synthase (eNOS) activity which is responsible for NO generation and cellular insulin-signaling. Hence, we examined the effects of IH on caveolin-1, eNOS, and endothelin-1 in human coronary artery endothelial cells in the context of IR. Chronic 3-day IH exposure up-regulated caveolin-1</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Intermittent hypoxia regulates vasoactive molecules and alters insulin-signaling in vascular endothelial cells.</pubmed_title><pmcid>PMC6148090</pmcid><funding_grant_id>17GRNT33660138</funding_grant_id><funding_grant_id>HL65176</funding_grant_id><funding_grant_id>R01 HL065176</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Sharma P</pubmed_authors><pubmed_authors>Dong Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Peterson TE</pubmed_authors><pubmed_authors>Singh P</pubmed_authors><pubmed_authors>Somers VK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Intermittent hypoxia regulates vasoactive molecules and alters insulin-signaling in vascular endothelial cells.</name><description>Vascular dysfunction and insulin resistance (IR) are associated with obstructive sleep apnea (OSA), which is characterized by frequent episodes of nocturnal intermittent hypoxia (IH). While it is recognized that the balance between vasoconstrictive (endothelin-1) and vasodilatory molecules (nitric oxide, NO) determine vascular profile, molecular mechanisms contributing to vascular dysfunction and IR in OSA are not completely understood. Caveolin-1 is a membrane protein which regulates endothelial nitric oxide synthase (eNOS) activity which is responsible for NO generation and cellular insulin-signaling. Hence, we examined the effects of IH on caveolin-1, eNOS, and endothelin-1 in human coronary artery endothelial cells in the context of IR. Chronic 3-day IH exposure up-regulated caveolin-1</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Sep</publication><modification>2025-04-04T20:15:30.152Z</modification><creation>2025-04-04T20:15:30.152Z</creation></dates><accession>S-EPMC6148090</accession><cross_references><pubmed>30237409</pubmed><doi>10.1038/s41598-018-32490-3</doi></cross_references></HashMap>