Open AccessSIRT1 confers protection against ischemia/reperfusion injury in cardiomyocytes via regulation of uncoupling protein 2 expression
Author(s) -
Min Deng,
Daxin Wang,
Shenghu He,
Rixin Xu,
Yuanyuan Xie
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7452
Subject(s) - sirtuin 1 , gene knockdown , ischemia , reperfusion injury , hypoxia (environmental) , myocardial infarction , biology , uncoupling protein , apoptosis , in vivo , sirtuin , pharmacology , medicine , downregulation and upregulation , endocrinology , chemistry , nad+ kinase , gene , biochemistry , enzyme , microbiology and biotechnology , organic chemistry , oxygen , brown adipose tissue , obesity
The development of a novel targeted therapy for acute myocardial infarction (AMI) remains a major hurdle in the treatment of cardiovascular disease. Previous studies indicate that mitochondrial uncoupling protein 2 (UCP‑2) is involved in the progression of AMI. The present study uses lentivirus knockdown of Sirtuin 1 (SIRT1) in H9c2 cells under hypoxia conditions, and revealed that levels of SIRT1 are accompanied by the expression of UCP‑2. Therefore, it was hypothesized that SIRT1 might be important in the development of myocardial infarction. The present study demonstrated that: i) exogenous expression of SIRT1 in vitro induced resistance to hypoxic injury in H9c2 cells, coinciding with a reduction in expression of UCP‑2; ii) knockdown of UCP‑2 conferred resistance to hypoxic injury in H9c2; iii) intraperitoneal injection of resveratrol and the resultant increase in SIRT1 levels may protect against ischemia/reperfusion injury in vivo, concomitant with decreased expression of UCP‑2. These findings provide direct evidence that the SIRT1/UCP‑2 axis might be important in myocardial infarction, and suggest that this axis may be a novel therapeutic target for the treatment of cardiovascular disease.