CIRP downregulation renders cardiac cells prone to apoptosis in heart failure.

Abstract

OBJECTIVES:

Cold-inducible RNA binding protein (CIRP) is a stress protein which is involved in regulating multiple cellular processes. However, its role in pathological heart diseases is still unknown. Our current study was aimed at addressing the response and functional role of CIRP in heart failure.

METHODS:

CIRP protein level was evaluated in heart samples from patients with heart failure and mice with post-myocardial infarction (post-MI). Cardiac-derived H9C2 cells were utilized to test the effects of CIRP deficiency on cell survival and apoptosis in response to H2O2 treatment.

RESULTS:

Reduced expression of cardiac CIRP was observed in patients with heart failure, mice with post-MI. In addition, knockdown of CIRP exacerbated cell apoptosis and cell death in response to H2O2 treatment, suggesting a protective role of CIRP in cell apoptosis induced by oxidative stress in the heart.

CONCLUSIONS:

Our findings suggest that altered expression of CIRP may be involved in the pathogenesis of heart failure and downregulation of CIRP may render cardiac cells prone to apoptosis in heart failure.

• Authors: Minxiao Chen, Hui Fu, Jingjing Zhang, He Huang, Peng Zhong
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 517 Issue 4 Pg. 545-550 (10 01 2019) ISSN: 1090-2104 [Electronic] United States
• PMID: 31405566 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2019. Published by Elsevier Inc.

Chemical References

• CIRBP protein, human
• Cirbp protein, mouse
• RNA-Binding Proteins
• Hydrogen Peroxide

Topics

• Animals
• Apoptosis (drug effects)
• Cell Line
• Disease Models, Animal
• Down-Regulation (drug effects)
• Heart Failure (metabolism, pathology)
• Humans
• Hydrogen Peroxide (toxicity)
• Male
• Mice, Inbred C57BL
• Myocardial Infarction (metabolism, pathology)
• Myocytes, Cardiac (drug effects, metabolism, pathology)
• RNA-Binding Proteins (metabolism)
• Rats