Silencing of angiotensin‑converting enzyme by RNA interference prevents H9c2 cardiomyocytes from apoptosis induced by anoxia/reoxygenation through regulation of the intracellular renin-angiotensin system

Int J Mol Med. 2013 Dec;32(6):1380-6. doi: 10.3892/ijmm.2013.1525. Epub 2013 Oct 11.

Abstract

Inhibition of the angiotensin‑converting enzyme (ACE) attenuated apoptotic cardiomyocytes induced by ischemic reperfusion (I/R). However, it is difficult to evaluate the effects of inhibition of the intracellular ACE in vivo. The objective of this study was to determine whether the apoptosis in H9c2 cardiomyocytes following anoxia/reoxygenation (A/R) would be improved by the silencing of intracellular ACE by RNA interference (RNAi). H9c2 cardiomyocytes were subjected to A/R 48 h following transfection with ACE-shRNA plasmid. The results showed that the gene silencing of intracellular ACE significantly inhibited the decrease of cell viability and the increase of apoptotic H9c2 cardiomyocytes undergoing A/R. Additionally, the gene silencing of intracellular ACE significantly promoted the expression of ACE2, decreased caspase‑3 activity and Bax levels, and enhanced the expression of Bcl‑2 in H9c2 cardiomyocytes subjected to A/R. The results suggest that the gene silencing of intracellular ACE holds great potential in the treatment of cardiomyocyte apoptosis following I/R injury through the regulation of the intracellular renin‑angiotensin system, thereby regulating the intrinsic pathway of apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / metabolism
  • Animals
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Cell Hypoxia / drug effects
  • Cell Survival / drug effects
  • Fluorescence
  • Intracellular Space / drug effects
  • Intracellular Space / metabolism
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Myocytes, Cardiac / cytology*
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / enzymology*
  • Oxygen / pharmacology*
  • Peptidyl-Dipeptidase A / genetics
  • Peptidyl-Dipeptidase A / metabolism*
  • RNA Interference / drug effects*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Renin-Angiotensin System / drug effects*
  • Transfection
  • bcl-2-Associated X Protein / metabolism

Substances

  • RNA, Messenger
  • bcl-2-Associated X Protein
  • Angiotensin II
  • Peptidyl-Dipeptidase A
  • Caspase 3
  • Oxygen