http://purl.uniprot.org/citations/28957873 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/28957873 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundRemifentanil postconditioning (RPC) confers robust cardioprotection against ischemia/reperfusion (I/R) injury. We recently determined that HDAC3 was involved in RPC-induced cardioprotection. However, the role of HDAC3 and its possible mechanisms in RPC-induced cardioprotection are unknown, which we aimed to evaluate in an in vitro hypoxia/reoxygenation (HR) model.MethodsMyocardium I/R injury was established after HR with H9c2 cardiomyoblasts. Cell viability and apoptosis were evaluated usingCCK-8 and flow cytometry of HR-injured cardiomyoblasts treated with or without RPC. Furthermore, effects of RPC on HDAC3 protein and mRNA expression were evaluated with Western blot and quantitative real-time PCR analyses, whereas GSK-3β expression was measured with Western blot.ResultsRPC increased cell viability and reduced cell apoptosis (P < 0.05) in H9c2 cardiomyoblasts subjected to HR injury. In addition, RPC promoted the phosphorylation of GSK-3β at Ser9 site (P < 0.05) and suppressed the protein and mRNA expression of HDAC3 (P < 0.05). Lentiviral-transduced overexpression of HDAC3 had no significant effects on HR injury while attenuating the cardioprotective effects of RPC on cell viability and apoptosis (P < 0.05), GSK-3β phosphorylation (P < 0.05) in H9c2 cardiomyoblasts.ConclusionsRPC attenuates apoptosis in H9c2 cardiomyoblasts after HR injury by downregulating HDAC3-mediated phosphorylation of GSK-3β. Our findings suggest that HDAC3, and its cross talk function with GSK-3β, may be a promising target for myocardium I/R injury."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.org/dc/terms/identifier | "doi:10.1097/shk.0000000000001008"xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Chen L."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Cheng X."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Chen M."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Liu Q."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/author | "Gu E."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/name | "Shock"xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/pages | "240-247"xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/title | "HDAC3 Mediates Cardioprotection of Remifentanil Postconditioning by Targeting GSK-3beta in H9c2 Cardiomyocytes in Hypoxia/Reoxygenation Injury."xsd:string |
http://purl.uniprot.org/citations/28957873 | http://purl.uniprot.org/core/volume | "50"xsd:string |
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