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http://purl.uniprot.org/citations/28957873http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28957873http://www.w3.org/2000/01/rdf-schema#comment"

Background

Remifentanil 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.

Methods

Myocardium 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.

Results

RPC 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.

Conclusions

RPC 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/28957873http://purl.org/dc/terms/identifier"doi:10.1097/shk.0000000000001008"xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Cheng X."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Chen M."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/author"Gu E."xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/name"Shock"xsd:string
http://purl.uniprot.org/citations/28957873http://purl.uniprot.org/core/pages"240-247"xsd:string
http://purl.uniprot.org/citations/28957873http://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/28957873http://purl.uniprot.org/core/volume"50"xsd:string
http://purl.uniprot.org/citations/28957873http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28957873
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