Effeet of rapamycin on mTOR and eIF-4E expression in coxsackievirus B3-induced rat myocardial cells.
- Author:
Chun-Yuan CHEN
1
;
Yue-Nu SUN
;
Zuo-Cheng YANG
Author Information
1. Department of Pediatics, Third Xiangya Hospital, Central South University, Changsha 410013, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Coxsackievirus Infections;
Enterovirus B, Human;
Eukaryotic Initiation Factor-4E;
biosynthesis;
Myocarditis;
metabolism;
virology;
Myocytes, Cardiac;
metabolism;
Protein Kinases;
biosynthesis;
Rats;
Rats, Sprague-Dawley;
Signal Transduction;
Sirolimus;
pharmacology;
TOR Serine-Threonine Kinases
- From:
Journal of Central South University(Medical Sciences)
2008;33(7):612-617
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To observe the effeet of rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), on mTOR and eukaryotic initiation factor-4E(eIF-4E)expression in coxsac-kievirus B3 (CVB3)-induced rat myocardial cells and to investigate the role of mTOR/eIF-4E signal pathway in viral myocarditis.
METHODS:To construct a cell model of viral myocarditis with primary cultured myocardial cells. Myocardial cells infected by CVB3 were treated with 10 nmol/L rapamycin according to the cell toxicity test. The mTOR and eIF-4E expressions of cells were determined by RT-PCR and Western Blot.
RESULTS:Rapamycin inhibited the degeneration of CVB3-induced myocardial cells. Expressions of mTOR and eIF-4E mRNA or protein in CVB3-induced myocardial cells were significantly upregulated compared with the control group (P < 0.05), and rapamycin (10 nmol/L) inhibited the upregulation (P < 0.05).
CONCLUSION:Rapamycin can downregulate the expressions of mTOR and eIF-4E in CVB3-induced myocardial cells, suggesting that mTOR/eIF-4E signal transduction may play an important role in viral myocarditis.
