Irisin Ameliorates Hypoxia/Reoxygenation-Induced Injury through Modulation of Histone Deacetylase 4

• DOI: 10.1371/journal.pone.0166182
• Publication Date: 2016-11-22T18:32:56Z
• Authors: Yu Tina Zhao; Hao Wang; Shouyan Zhang; Jianfeng Du; Shougang Zhuang; Ting C. Zhao
• Keywords: Myokine; HDAC4; Hypoxia; Annexin A5

Irisin is a recently identified myokine which brings increases in energy expenditure and contributes to the beneficial effects of exercise through browning white adipose tissues. However, its heart remains unknown. This study sought determine irisin on hypoxia/reoxygenation injury relationship with HDAC4. Wild type stable HDAC4-overexpression cells were generated from H9c2 cardiomyoblasts. HDAC4 overexpression wild exposed 24 hours hypoxia followed by one hour reoxygenation vitro presence or absence (5 ng/ml). Cell cytotoxicity, apoptosis, mitochondrial respiration, permeability transition pore (mPTP) determined. Western blotting was employed active-caspase 3, annexin V, expression. As compared group, remarkably led great increase cell death as evident increased lactate dehydrogenase (LDH) leakage, ratio caspase-3-positive well upregulated levels 3 V shown western blot analysis. In addition, also induced much severe dysfunction, indicated apoptotic mitochondria mPTP. treatment significantly attenuated all these effects. Though did not influence expression at transcriptional level, analysis showed that protein decreased time-dependent way after administration irisin, associated degradation mediated small ubiquitin-like modification (SUMO). Our results are first demonstrate protective cardiomyoblasts might be degradation.