Abstract 17980: Irisin Protects Against Hypoxia and Reoxygenation Injury Through Hdac4
Introduction: Irisin is a recently identified myokine that brings increases in energy expenditure and contributes to the beneficial effects of exercise on the browning of white adipose tissues. However, its effects in hearts remains unknown.
Hypothesis: This study sought to determine the effects of irisin on hypoxia/reoxygenation injury and its relationship with HDAC4.
Methods: Wild type and stable HDAC4-overexpression cells were generated from H9c2 cardiomyoblasts. HDAC4 overexpression cells and wild type H9c2 cells were exposed to 24 hours of hypoxia followed by one hour of reoxygenation in vitro in the presence or absence of irisin (10ng/ml). Cell cytotoxicity, apoptosis, mitochondrial respiration, and mitochondrial permeability transition pore (mPTP) were determined.
Results: As compared to wild type H9c2 cells subjected to normoxia, hypoxia treatments resulted in an increase in the cell death as evident by the increase in lactate dehydrogenase (LDH) leakage, caspase-3 positive cells, apoptotic mitochondria, and increased mPTP , which were attenuated by irisin treatment. However, the irisin-induced improvement in reduction in cell death and improvement in mitochondrial function were suppressed in HDAC4 overexpression cardiomyoblasts exposed to hypoxia and reoxygenation.
Conclusion: These results indicate that irisin produces protective effects against hypoxia/reoxygenation injury, which is dependent upon HDAC4.
Author Disclosures: Y.T. Zhao: None. J. Du: None. H. Wang: None. L. Zhang: None. T.C. Zhao: None.
- © 2016 by American Heart Association, Inc.