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Adiponectin Attenuates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury Through Inhibition of Endoplasmic Reticulum Stress
  1. Yun-fei Bian, MD,
  2. Xiao-yan Hao, MD,
  3. Feng Gao, MD,
  4. Hui-yu Yang, MD,
  5. Nana Zang, MD,
  6. Chuan-shi Xiao, MD
  1. From the Department of Cardiology, The Second Hospital of Shanxi Medical University, Taiyuan, China.
  1. Received September 12, 2010, and in revised form February 21, 2011.
  2. Accepted for publication February 21, 2011.
  3. Reprints: Chuan-shi Xiao, MD, Department of Cardiology, The Second Hospital of Shanxi Medical University, 382 Wuyi Road, Taiyuan 030001, China. E-mail: chuan01shi08xiao10{at}googlemail.com.

Abstract

Adiponectin (APN) is a potent cardioprotective molecule. The present study aims to investigate the underlying mechanism(s) for its cardioprotective effect. We isolated primary cardiomyocytes from neonatal rats and established an in vitro model of hypoxia/reoxygenation (H/R). The cardiomyocytes were randomly divided into 6 groups: saline group (control), dithiothreitol group (5 mM dithiothreitol for 2 hours), H/R group, H/R + APN group (incubation with 30 μg/mL APN, followed by H/R), H/R + APN + SB203580 (SB) group (treatment with 30 μg/mL APN and 5 μM SB, followed by H/R), and H/R + SB group (exposure to 5 μM SB and then H/R). Cell death was detected by measuring lactate dehydrogenase release. The expression levels of hypoxia-inducible factor 1α and endoplasmic reticulum stress-related genes including GRP78, caspase-12, C/EBP homologous protein, and p38 mitogen-activated protein kinase were examined. Cardiomyocytes exposed to H/R showed a significant increase in lactate dehydrogenase leakage and hypoxia-inducible factor 1α protein levels compared with the control cells (P < 0.05). The H/R-provoked cell death was profoundly attenuated by the pretreatment with APN alone, SB alone, or both, which was coupled with decreased expression of GRP78, caspase-12, C/EBP homologous protein, and p38 mitogen-activated protein kinase. These results provide new insights into the mechanism of APN-mediated cardioprotection, which may be partially due to inhibition of endoplasmic reticulum stress response.

Key Words
  • adiponectin
  • hypoxia-reoxygenation
  • endoplasmic reticulum stress
  • p38 MAPK
  • cell death
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