title: 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.
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.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, P.R. China.
authors.forename: Weiguo
authors.initials: W
authors.lastname: Wan
authors.forename: Xuejun
authors.initials: X
authors.lastname: Jiang
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Li
authors.forename: Cui
authors.initials: C
authors.lastname: Zhang
authors.forename: Xin
authors.initials: X
authors.lastname: Yi
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D015687:Cell Hypoxia / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D005453:Fluorescence; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000187:drug effects / Q000201:enzymology*; D010100:Oxygen / Q000494:pharmacology*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference / Q000187:drug effects*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D012084:Renin-Angiotensin System / Q000187:drug effects*; D014162:Transfection; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; D053148:Caspase 3; D010100:Oxygen