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dc.contributor.authorAhmed, Suhail
dc.contributor.authorKurusamy, Sathishkumar
dc.contributor.authorDavid, Ezra Leander Santhosh
dc.contributor.authorKhan, Kinza
dc.contributor.authorKalyanakrishnan, Krithika
dc.contributor.authorIan-Gobo, Miebaka
dc.contributor.authorKola, Teja Manidhar
dc.contributor.authorWilkinson, Robert N
dc.contributor.authorKannappan, Vinodh
dc.contributor.authorWang, Weiguang
dc.contributor.authorGómez, Manuel J
dc.contributor.authorRedondo, Juan Miguel
dc.contributor.authorCotton, James
dc.contributor.authorArmesilla, Angel
dc.date.accessioned2022-08-31T09:56:14Z
dc.date.available2022-08-31T09:56:14Z
dc.date.issued2022-08-30
dc.identifier.citationAhmed, S., Kurusamy, S., David, E.L.S. et al. (2022) Aberrant expression of miR-133a in endothelial cells inhibits angiogenesis by reducing pro-angiogenic but increasing anti-angiogenic gene expression. Scientific Reports 12, 14730. https://doi.org/10.1038/s41598-022-19172-xen
dc.identifier.issn2045-2322en
dc.identifier.doi10.1038/s41598-022-19172-xen
dc.identifier.urihttp://hdl.handle.net/2436/624913
dc.description© 2022 The Authors. Published by Springer. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.1038/s41598-022-19172-xen
dc.description.abstractAngiogenesis is a multi-factorial physiological process deregulated in human diseases characterised by excessive or insufficient blood vessel formation. Emerging evidence highlights a novel role for microRNAs as regulators of angiogenesis. Previous studies addressing the effect of miR-133a expression in endothelial cells during blood vessel formation have reported conflicting results. Here, we have assessed the specific effect of mature miR-133a strands in angiogenesis and the expression of endothelial angiogenic genes. Transfection of miR-133a-3p or -5p mimics in primary human endothelial cells significantly inhibited proliferation, migration, and tubular morphogenesis of transfected cells. Screening of gene arrays related to angiogenic processes, and further validation by TaqMan qPCR, revealed that aberrant expression of miR-133a-3p led to a decrease in the expression of genes encoding pro-angiogenic molecules, whilst increasing those with anti-angiogenic functions. Ingenuity Pathway Analysis of a collection of genes differentially expressed in cells harbouring miR-133a-3p, predicted decreased cellular functions related to vasculature branching and cell cycle progression, underlining the inhibitory role of miR-133a-3p in angiogenic cellular processes. Our results suggest that controlled delivery of miR-133a-3p mimics, or antagomirs in diseased endothelial cells, might open new therapeutic interventions to treat patients suffering from cardiovascular pathologies that occur with excessive or insufficient angiogenesis.en
dc.description.sponsorshipThis work was supported by the Research Institute in Healthcare Sciences, Faculty of Science and Engineering, University of Wolverhampton (to A.L.A) and by generous donations from the charities “Wolverhampton Coronary Aftercare Support Group” (to A.L.A and J.C) and “Rotha Abraham Bequest” (to A.L.A and J.C). S.A. is the recipient of a University of Wolverhampton-Wolverhampton Royal NHS Trust joint PhD studentship. JMR has received funding from the “La Caixa” Banking Foundation HR18-00068 (to J.M.R.); Spanish Ministerio de Ciencia e Innovación grant RTI2018-099246-B-I00 (MICIU/AEI/FEDER, UE) to J.M.R and the Instituto de Salud Carlos III (CIBER-CV CB16/11/00264) to J.M.R. The Centro Nacional de Investigaciones Cardiovasculares (CNIC) is supported by the Spanish Ministry of Economy, Industry and Competitiveness (MEIC) and the Pro-CNIC Foundation.en
dc.formatapplication/pdfen
dc.languageen
dc.language.isoenen
dc.publisherSpringeren
dc.relation.urlhttps://www.nature.com/articles/s41598-022-19172-xen
dc.subjectangiogenesisen
dc.subjectmicroRNAen
dc.titleAberrant expression of miR-133a in endothelial cells inhibits angiogenesis by reducing pro-angiogenic but increasing anti-angiogenic gene expressionen
dc.typeJournal articleen
dc.identifier.eissn2045-2322
dc.identifier.journalScientific Reportsen
dc.date.updated2022-08-30T13:35:24Z
dc.date.accepted2022-08-25
rioxxterms.funderWolverhampton Coronary Aftercare Support Group, Rotha Abraham Bequest, University of Wolverhampton, Wolverhampton Royal NHS Trust, “La Caixa” Banking Foundation, Spanish Ministerio de Ciencia e Innovación, Instituto de Salud Carlos III, Spanish Ministry of Economy, Industry and Competitiveness (MEIC), Pro-CNIC Foundation.en
rioxxterms.identifier.projectHR18-00068, RTI2018-099246-B-I00 (MICIU/AEI/FEDER, UE), CIBER-CV CB16/11/00264en
rioxxterms.versionVoRen
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/en
rioxxterms.licenseref.startdate2022-08-31en
dc.source.volume12
dc.source.issue1
dc.description.versionPublished online
refterms.dateFCD2022-08-31T09:55:52Z
refterms.versionFCDVoR
refterms.dateFOA2022-08-31T09:56:15Z


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