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Downregulation of RACK1 is associated with cardiomyocyte apoptosis after myocardial ischemia/reperfusion injury in adult rats

  • Long Qian
  • Jiahai Shi
  • Chi Zhang
  • Jiawei Lu
  • Xiaoning Lu
  • Kunpeng Wu
  • Chen Yang
  • Daliang Yan
  • Chao Zhang
  • Qingsheng YouEmail author
  • Xiaojuan LiuEmail author
Article

Abstract

The receptor for activated C kinase 1 (RACK1) is a multifaceted scaffolding protein that mediates the shuttling of activated protein kinase C (PKC) to cellular membranes. In addition, RACK1 could decrease cell apoptosis in a variety of disease models. However, the function of RACK1 in cardiomyocyte apoptosis after myocardial ischemia/reperfusion (I/R) is unknown. In this study, male Sprague–Dawley rats were anesthetized and subjected to myocardial I/R insult consisting of 30 min left anterior descending coronary artery (LAD) occlusion followed by reperfusion for 1, 2, 4, 6, 8, 12, and 24 h. The expression of RACK1 was decreased after myocardial I/R and was associated with cardiomyocyte apoptosis. To further verify the relationship between RACK1 and cardiomyocyte apoptosis, H9c2 cardiomyocytes were cultured under hypoxia for 6 h, then maintained in the regular incubator to reoxygenation. After H9c2 cells were transfected with Flag-RACK1 to overexpress RACK1, RACK1 expression was upregulated in hypoxia/reoxygenation (H/R) 4 h group accompanied with the decrease of cleaved caspase-3 and the increase of Bcl-2 expression. Terminal transferase-mediated biotin dUTP nick end labeling (TUNEL) assay showed that RACK1 overexpression inhibited H9c2 cell apoptosis induced by H/R treatment. Our data suggested that RACK1 might suppress cardiomyocyte apoptosis after I/R, providing a novel molecular target for the therapy of ischemia heart disease.

Keywords

Myocardial ischemia/reperfusion Apoptosis RACK1 Rats 

Notes

Acknowledgments

This work was supported in part by the National Natural Science Foundation of China (Nos. 81401365, 81373223, 81200918, and 81172879), a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD).

Compliance with ethical standards

Conflicts of interest

The authors declare that they have no conflict of interest.

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Copyright information

© The Society for In Vitro Biology 2015

Authors and Affiliations

  • Long Qian
    • 1
    • 4
  • Jiahai Shi
    • 1
    • 4
  • Chi Zhang
    • 2
    • 4
  • Jiawei Lu
    • 1
    • 4
  • Xiaoning Lu
    • 1
    • 4
  • Kunpeng Wu
    • 1
    • 4
  • Chen Yang
    • 1
    • 4
  • Daliang Yan
    • 1
    • 4
  • Chao Zhang
    • 2
    • 4
  • Qingsheng You
    • 1
    • 4
    Email author
  • Xiaojuan Liu
    • 3
    • 4
    Email author
  1. 1.Department of Thoracic SurgeryAffiliated Hospital of Nantong UniversityNantongPeople’s Republic of China
  2. 2.Department of VasculocardiologyAffiliated Hospital of Nantong UniversityNantongPeople’s Republic of China
  3. 3.Department of Pathogen Biology, Medical CollegeNantong UniversityNantongPeople’s Republic of China
  4. 4.Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical CollegeNantong UniversityNantongPeople’s Republic of China

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