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dc.contributor.authorTurczyńska, Karolina M.
dc.contributor.authorSwärd, Karl
dc.contributor.authorThi Hien, Tran
dc.contributor.authorWohlfahrt, Johan
dc.contributor.authorMattisson, Ingrid Yao
dc.contributor.authorEkman, Mari
dc.contributor.authorNilsson, Johan
dc.contributor.authorSjögren, Johan
dc.contributor.authorMurugesan, Vignesh
dc.contributor.authorHultgårdh-Nilsson, Anna
dc.contributor.authorCidad Velasco, María del Pilar
dc.contributor.authorHellstrand, Per
dc.contributor.authorPérez García, María Teresa 
dc.contributor.authorAlbinsson, Sebastian
dc.date.accessioned2020-12-22T08:55:51Z
dc.date.available2020-12-22T08:55:51Z
dc.date.issued2015
dc.identifier.citationArteriosclerosis, Thrombosis, and Vascular Biology, 2015, vol. 35, n. 6. p. 1489-1497es
dc.identifier.issn1524-4636es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/44592
dc.descriptionProducción Científicaes
dc.description.abstractObjective: Actin dynamics in vascular smooth muscle is known to regulate contractile differentiation and may play a role in the pathogenesis of vascular disease. However, the list of genes regulated by actin polymerization in smooth muscle remains incomprehensive. Thus, the objective of this study was to identify actin-regulated genes in smooth muscle and to demonstrate the role of these genes in the regulation of vascular smooth muscle phenotype. Approach and Results: Mouse aortic smooth muscle cells were treated with an actin-stabilizing agent, jasplakinolide, and analyzed by microarrays. Several transcripts were upregulated including both known and previously unknown actin-regulated genes. Dystrophin and synaptopodin 2 were selected for further analysis in models of phenotypic modulation and vascular disease. These genes were highly expressed in differentiated versus synthetic smooth muscle and their expression was promoted by the transcription factors myocardin and myocardin-related transcription factor A. Furthermore, the expression of both synaptopodin 2 and dystrophin was significantly reduced in balloon-injured human arteries. Finally, using a dystrophin mutant mdx mouse and synaptopodin 2 knockdown, we demonstrate that these genes are involved in the regulation of smooth muscle differentiation and function. Conclusions: This study demonstrates novel genes that are promoted by actin polymerization, that regulate smooth muscle function, and that are deregulated in models of vascular disease. Thus, targeting actin polymerization or the genes controlled in this manner can lead to novel therapeutic options against vascular pathologies that involve phenotypic modulation of smooth muscle cells.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherAmerican Heart Associationes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/*
dc.subject.classificationAngioplastyes
dc.subject.classificationAngioplastiaes
dc.subject.classificationGene expressiones
dc.subject.classificationExpresión génicaes
dc.subject.classificationVascular diseaseses
dc.subject.classificationEnfermedades vasculareses
dc.titleRegulation of smooth muscle dystrophin and synaptopodin 2 expression by actin polymerization and vascular injuryes
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2015 American Heart Associationes
dc.identifier.doi10.1161/ATVBAHA.114.305065es
dc.relation.publisherversionhttps://www.ahajournals.org/doi/10.1161/ATVBAHA.114.305065es
dc.peerreviewedSIes
dc.description.projectInstituto de Salud Carlos III - Fondo Europeo de Desarrollo Regional (grant RD12/0042/0006)es
dc.description.projectMinisterio de Economía, Industria y Competitividad (grants BFU2010-15898 and BFU2013-45867-R)es
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Unported*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones
dc.subject.unesco32 Ciencias Médicases


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