Ischemia-reperfusion injury up-regulates Pim-3 gene expression in myocardial tissue.
10.1007/s11596-010-0644-9
- Author:
Libing ZHAO
1
;
Yinfang WANG
;
Xinwen MIN
;
Handong YANG
;
Peng ZHANG
;
Qiutang ZENG
Author Information
1. Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. zhaolibing@medmail.com.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Male;
Myocardial Ischemia;
metabolism;
physiopathology;
Myocardial Reperfusion Injury;
metabolism;
Myocardium;
metabolism;
Oxidative Stress;
physiology;
Protein-Serine-Threonine Kinases;
genetics;
metabolism;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
Up-Regulation
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2010;30(6):704-708
- CountryChina
- Language:English
-
Abstract:
This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.
