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HDAC3 Mediates Cardioprotection of Remifentanil Post-Conditioning by Targeting GSK-3β In H9c2 Cardiomyocytesin Hypoxia/Reoxygenation Injury.

HDAC3 Mediates Cardioprotection of Remifentanil Post-Conditioning by Targeting GSK-3β In H9c2 Cardiomyocytesin Hypoxia/Reoxygenation Injury.
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Chen M, Qin L, Chen L, Zhang L, Cheng X, Gu E,


Chen M, Qin L, Chen L, Zhang L, Cheng X, Gu E, (click to view)

Chen M, Qin L, Chen L, Zhang L, Cheng X, Gu E,

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Shock (Augusta, Ga.) 2017 09 27() doi 10.1097/SHK.0000000000001008
Abstract
BACKGROUND
Remifentanil post-conditioning (RPC) confers robust cardioprotection againstis chemia/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 following 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, while 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 attenuated 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 crosstalk function with GSK-3β, may be a promising target for myocardium I/R injury.

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