Calreticulin-induced mitochondrial injury: a novel mechanism of cardiac hypertrophy.
- Author:
Hu SHAN
1
;
Jin WEI
;
Ming ZHANG
;
Rui YAN
;
Lin LIN
;
Rong ZHANG
;
Yanhe ZHU
;
Wuhong TAN
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Calreticulin; metabolism; Cardiomegaly; Cells, Cultured; Membrane Potential, Mitochondrial; Mitochondria; pathology; Myocytes, Cardiac; pathology; Protein Biosynthesis; RNA, Small Interfering; Rats
- From: Journal of Southern Medical University 2014;34(9):1248-1253
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of angiotensin II (Ang II) on calreticulin (CRT) expression and its association with mitochondrial dysfunction in cardiomyocytes.
METHODSPrimary neonatal rat cardiomyocytes were randomly divided into CRT siRNA group, control siRNA group, control group, Ang II+ CRT siRNA group, Ang II+ control siRNA group and Ang II group. The cell surface area, protein synthesis rate, mitochondrial membrane potential level, enzyme activities, and CRT expression were observed.
RESULTSCompared with those in the control group, the cell surface area and protein synthesis rate were both increased and mitochondrial membrane potential level and enzyme activities decreased in Ang II groups. CRT expression was significantly down-regulated in Ang II+ CRT siRNA group with increased cell surface area, protein synthesis rate, mitochondrial membrane potential level and enzyme activities as compared with those in Ang II+ control siRNA group.
CONCLUSIONAng II up-regulates CRT expression to induce mitochondrial injury, which may be an important mechanism of myocardial hypertrophy.