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http://purl.uniprot.org/citations/24974728http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24974728http://www.w3.org/2000/01/rdf-schema#comment"Stem-cell antigen 1-positive (Sca-1+) cardiac stem cells (CSCs), a vital kind of CSCs in humans, promote cardiac repair in vivo and can differentiate to cardiomyocytes with 5'-azacytizine treatment in vitro. However, the underlying molecular mechanisms are unknown. β-arrestin2 is an important scaffold protein and highly expressed in the heart. To explore the function of β-arrestin2 in Sca-1+ CSC differentiation, we used β-arrestin2-knockout mice and overexpression strategies. Real-time PCR revealed that β-arrestin2 promoted 5'-azacytizine-induced Sca-1+ CSC differentiation in vitro. Because the microRNA 155 (miR-155) may regulate β-arrestin2 expression, we detected its role and relationship with β-arrestin2 and glycogen synthase kinase 3 (GSK3β), another probable target of miR-155. Real-time PCR revealed that miR-155, inhibited by β-arrestin2, impaired 5'-azacytizine-induced Sca-1+ CSC differentiation. On luciferase report assay, miR-155 could inhibit the activity of β-arrestin2 and GSK3β, which suggests a loop pathway between miR-155 and β-arrestin2. Furthermore, β-arrestin2-knockout inhibited the activity of GSK3β. Akt, the upstream inhibitor of GSK3β, was inhibited in β-arrestin2-Knockout mice, so the activity of GSK3β was regulated by β-arrestin2 not Akt. We transplanted Sca-1+ CSCs from β-arrestin2-knockout mice to mice with myocardial infarction and found similar protective functions as in wild-type mice but impaired arterial elastance. Furthermore, low level of β-arrestin2 agreed with decreased phosphorylation of AKT and increased phophorylation of GSK3β, similar to in vitro findings. The β-arrestin2/miR-155/GSK3β pathway may be a new mechanism with implications for treatment of heart disease."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.org/dc/terms/identifier"doi:10.1111/jcmm.12339"xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Feng Y."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Zhao J."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Yan H."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Yin D."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Stuart C."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/author"Chua B."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/name"J Cell Mol Med"xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/pages"1562-1570"xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/title"beta-arrestin2/miR-155/GSK3beta regulates transition of 5'-azacytizine-induced Sca-1-positive cells to cardiomyocytes."xsd:string
http://purl.uniprot.org/citations/24974728http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/24974728http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24974728
http://purl.uniprot.org/citations/24974728http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24974728
http://purl.uniprot.org/uniprot/Q91YI4#attribution-15A1C78797703CFD48FCD892EF8A078Fhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/Q91YI4#attribution-1EC92A7FFCF36239D7B0936D442B1598http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/Q91YI4#attribution-952C3153D1801774D0A55E04792EEACAhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/Q9WV60#attribution-15A1C78797703CFD48FCD892EF8A078Fhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/#_A0A158SIT9-mappedCitation-24974728http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/#_A0A338P6P8-mappedCitation-24974728http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24974728
http://purl.uniprot.org/uniprot/#_J3QN53-mappedCitation-24974728http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24974728