{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Samak M"],"funding":["Deutsche Sonderforschungsbereich","European Research Council"],"pagination":["58"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8773250"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"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"],"journal":["Biomedicines"],"pubmed_title":["Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes."],"pmcid":["PMC8773250"],"funding_grant_id":["CRC127","ERC StG 758087","758087"],"pubmed_authors":["Kues A","Le Noble F","Kaltenborn D","Hinkel R","Germena G","Samak M"],"additional_accession":[]},"is_claimable":false,"name":"Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes.","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","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2026-06-19T03:09:53.895Z","creation":"2022-02-11T16:04:54.476Z"},"accession":"S-EPMC8773250","cross_references":{"pubmed":["35052738"],"doi":["10.3390/biomedicines10010058"]}}