PMID- 19099956
OWN - NLM
STAT- MEDLINE
DCOM- 20090909
LR  - 20131121
IS  - 0253-3758 (Print)
IS  - 0253-3758 (Linking)
VI  - 36
IP  - 2
DP  - 2008 Feb
TI  - [Effects of mTOR inhibitor rapamycin on Smad 3 protein and collagen type I 
      expression in rat myocardial fibroblasts infected with coxsackie virus B 3].
PG  - 156-60
AB  - OBJECTIVE: Mammalian target of rapamycin (mTOR) plays a central role in 
      controlling cell proliferation, survival and growth. We investigated the role of 
      mTOR signal transduction on viral myocarditis by observing the effect of mTOR 
      inhibitor rapamycin on Smad 3 and collagen type I expression in rat myocardial 
      fibroblasts infected with coxsackievirus B 3 (CVB 3). METHODS: Primary cultured 
      myocardial fibroblasts of SD rats infected with CVB 3 were treated with or 
      without rapamycin. The Smad 3 and collagen type I expression of the cells were 
      determined by RT-PCR and Western blot. RESULTS: (1) mTOR/beta-actin ratio was 
      dose-dependently reduced (1 nmol/L, 0.381 +/- 0.022; 10 nmol/L, 0.282 +/- 0.014; 
      100 nmol/L, 0.263 +/- 0.012 vs. control 1.45 +/- 0.04, all P < 0.05 vs. control) 
      after 48 hours rapamycin treatments and time-dependently reduced after 10 nmol/L 
      rapamycin treatment (24 h, 0.203 +/- 0.021; 48 h, 0.163 +/- 0.022; 72 h, 0.144 
      +/- 0.013 vs. 0 h, 0.341 +/- 0.022, all P < 0.05 vs.0 h) in CVB 3 infected 
      myocardial fibroblasts. (2) Smad 3/beta-actin ratio of myocardial fibroblasts was 
      significantly increased in CVB 3 infected cardial fibroblasts and this increase 
      could be significantly attenuated by rapamycin (control, 0.63 +/- 0.06; CVB 3, 
      1.18 +/- 0.03; CVB 3 + Rapamycin, 0.77 +/- 0.08 by RT-PCR and 0.89 +/- 0.07, 2.27 
      +/- 0.13 and 0.131 +/- 0.013 by Western blot). Collagen type I/beta-actin ratio 
      was also significantly increased by CVB 3 and this increase could be reversed by 
      rapamycin (1.13 +/- 0.06, 1.303 +/- 0.012, 0.82 +/- 0.03 by RT-PCR). CONCLUSION: 
      Rapamycin can inhibit the Smad 3 and collagen type I expressions in CVB 3 
      infected myocardial fibroblasts suggesting that the mTOR signal pathway may play 
      an important role in the pathogenesis of CVB 3 induced myocardial fibrosis.
FAU - Chen, Chun-yuan
AU  - Chen CY
AD  - Department of Paediatric, Third Xiangya Hospital, Central South University, 
      Changsha 410003, China.
FAU - Sun, Yue-Nu
AU  - Sun YN
FAU - Yang, Zuo-cheng
AU  - Yang ZC
FAU - Cai, Zi-li
AU  - Cai ZL
LA  - chi
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhonghua Xin Xue Guan Bing Za Zhi
JT  - Zhonghua xin xue guan bing za zhi
JID - 7910682
RN  - 0 (Collagen Type I)
RN  - 0 (Smad3 Protein)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Collagen Type I/*metabolism
MH  - Coxsackievirus Infections/metabolism
MH  - Enterovirus
MH  - Female
MH  - Fibroblasts/*metabolism
MH  - Male
MH  - Myoblasts, Cardiac/*metabolism/virology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - Sirolimus/*pharmacology
MH  - Smad3 Protein/*metabolism
EDAT- 2008/12/23 09:00
MHDA- 2009/09/10 06:00
CRDT- 2008/12/23 09:00
PHST- 2008/12/23 09:00 [entrez]
PHST- 2008/12/23 09:00 [pubmed]
PHST- 2009/09/10 06:00 [medline]
PST - ppublish
SO  - Zhonghua Xin Xue Guan Bing Za Zhi. 2008 Feb;36(2):156-60.