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http://purl.uniprot.org/citations/23509692http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23509692http://www.w3.org/2000/01/rdf-schema#comment"MicroRNAs (miRNAs, miRs) have the potential to control stem cells fate decisions. The cardiac- and skeletal-muscle-specific miRNA, miR-1, can regulate embryonic stem cells differentiation to cardiac lineage by suppressing gene expression of alternative lineages. Accordingly, we hypothesized that overexpression of miR-1 may also promote cardiac gene expression in mesenchymal stem cells. Since Notch signaling could inhibit muscle differentiation, a process in contrast with the effect of miR-1, miR-1-mediated repression of Notch signaling may contribute to the observed effects of miR-1 in mesenchymal stem cells. Thus, mesenchymal stem cells were infected by lentiviral vectors carrying miR-1, and cells expressing miR-1 were selected. Alterations in Notch signaling and cardiomyocyte markers, Nkx2.5, GATA-4, cTnT, and CX43, were identified by Western blot in the infected cells on days 1, 7, and 14. Our study showed that the downstream target molecule of Notch pathway, Hes-1, was obviously decreased in mesenchymal stem cells modified with miR-1, and overexpression of miR-1 promotes the specific cardiac gene expression in the infected cells. Knockdown of Hes-1 leads to the same effects on cell lineage decisions. Our results indicated that miR-1 promotes the differentiation of MSCs into cardiac lineage in part due to negative regulation of Hes-1."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.org/dc/terms/identifier"doi:10.1155/2013/216286"xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Tang L."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Huang F."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Hu X.Q."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Pan J.Y."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Zhou S.H."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/author"Fang Z.F."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/name"Biomed Res Int"xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/pages"216286"xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/title"miR-1-mediated induction of cardiogenesis in mesenchymal stem cells via downregulation of Hes-1."xsd:string
http://purl.uniprot.org/citations/23509692http://purl.uniprot.org/core/volume"2013"xsd:string
http://purl.uniprot.org/citations/23509692http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23509692
http://purl.uniprot.org/citations/23509692http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23509692
http://purl.uniprot.org/uniprot/#_Q3UZZ2-mappedCitation-23509692http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23509692
http://purl.uniprot.org/uniprot/#_P35428-mappedCitation-23509692http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23509692
http://purl.uniprot.org/uniprot/#_Q3V1C5-mappedCitation-23509692http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23509692
http://purl.uniprot.org/uniprot/P35428http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23509692
http://purl.uniprot.org/uniprot/Q3UZZ2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23509692
http://purl.uniprot.org/uniprot/Q3V1C5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23509692