<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Samak M</submitter><funding>Deutsche Sonderforschungsbereich</funding><funding>European Research Council</funding><pagination>58</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8773250</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>Microvascular dysfunction is a pathological hallmark of diabetes, and is central to the ethology of diabetes-associated cardiac events. Herein, previous studies have highlighted the role of the vasoactive micro-RNA 92a (miR-92a) in small, as well as large, animal models. In this study, we explore the effects of miR-92a on mouse and human cardiac microvascular endothelial cells (MCMEC, HCMEC), and its underlying molecular mechanisms. Diabetic HCMEC displayed impaired angiogenesis and a pronounced inflammatory phenotype. Quantitative PCR (qPCR) showed an upregulation of miR-92a in primary diabetic HCMEC. Downregulation of miR-92a by antagomir transfection in diabetic HCMEC rescued angiogenesis and ameliorated diabetic endothelial bed inflammation. Furthermore, additional analysis of potentia</pubmed_abstract><journal>Biomedicines</journal><pubmed_title>Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes.</pubmed_title><pmcid>PMC8773250</pmcid><funding_grant_id>CRC127</funding_grant_id><funding_grant_id>ERC StG 758087</funding_grant_id><funding_grant_id>758087</funding_grant_id><pubmed_authors>Kues A</pubmed_authors><pubmed_authors>Le Noble F</pubmed_authors><pubmed_authors>Kaltenborn D</pubmed_authors><pubmed_authors>Hinkel R</pubmed_authors><pubmed_authors>Germena G</pubmed_authors><pubmed_authors>Samak M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes.</name><description>Microvascular dysfunction is a pathological hallmark of diabetes, and is central to the ethology of diabetes-associated cardiac events. Herein, previous studies have highlighted the role of the vasoactive micro-RNA 92a (miR-92a) in small, as well as large, animal models. In this study, we explore the effects of miR-92a on mouse and human cardiac microvascular endothelial cells (MCMEC, HCMEC), and its underlying molecular mechanisms. Diabetic HCMEC displayed impaired angiogenesis and a pronounced inflammatory phenotype. Quantitative PCR (qPCR) showed an upregulation of miR-92a in primary diabetic HCMEC. Downregulation of miR-92a by antagomir transfection in diabetic HCMEC rescued angiogenesis and ameliorated diabetic endothelial bed inflammation. Furthermore, additional analysis of potentia</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-06-19T03:09:53.895Z</modification><creation>2022-02-11T16:04:54.476Z</creation></dates><accession>S-EPMC8773250</accession><cross_references><pubmed>35052738</pubmed><doi>10.3390/biomedicines10010058</doi></cross_references></HashMap>