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CIRP downregulation renders cardiac cells prone to apoptosis in heart failure

Minxiao Chen1, Hui Fu2, Jingjing Zhang2

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, PR China; Department of Pharmacology, Jinhua Municipal Central Hospital, Jinhua, 321000, PR China.

Biochemical and Biophysical Research Communications
|August 14, 2019
PubMed
Abstract

Insights

Cold-inducible RNA binding protein (CIRP) protects heart cells from apoptosis during heart failure. Reduced CIRP levels worsen cell death from oxidative stress, indicating a crucial protective role.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Stress Response

Background:

  • Cold-inducible RNA binding protein (CIRP) is a known stress protein regulating cellular processes.
  • The specific role of CIRP in the context of pathological heart diseases, particularly heart failure, remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and functional significance of CIRP in the failing heart.
  • To elucidate the protective or detrimental effects of CIRP in cardiac cells under stress conditions relevant to heart failure.

Main Methods:

  • Assessed CIRP protein levels in cardiac tissue from human heart failure patients and post-myocardial infarction (MI) mouse models.
  • Utilized H9C2 cardiac cells to examine the impact of CIRP deficiency on cell survival and apoptosis following hydrogen peroxide (H2O2) induced oxidative stress.

Main Results:

  • Cardiac CIRP expression was significantly reduced in both human heart failure patients and post-MI mice.
  • Knockdown of CIRP in H9C2 cells led to increased apoptosis and cell death when exposed to H2O2.
  • These findings suggest a protective role for CIRP against oxidative stress-induced apoptosis in cardiac cells.

Conclusions:

  • Altered CIRP expression is implicated in the pathogenesis of heart failure.
  • Downregulation of CIRP compromises the resilience of cardiac cells to apoptosis, potentially contributing to heart failure progression.
Keywords:
CIRPCardiac pathologyCell apoptosisHeart failureOxidative stress

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