Effects of all-trans retinioc acid on expressions of COL1α2,MMP-2,TIMP-1, and signaling pathway in TGF-β1-simulated rat hepatic stellate cells
10.7652/jdyxb201706014
- VernacularTitle:全反式维甲酸对TGF-β1刺激的肝星状细胞COL1α2、MMP-2、TIMP-1以及信号通路的影响
- Author:
Ke CHEN
1
;
wang Jun XU
;
Qi ZHOU
;
qian Xue LI
;
de Xiu FAN
Author Information
1. 西安交通大学第二附属医院医用超声研究室
- Keywords:
all-trans retinoic acid(ATRA);
hepatic stellate cell (HSC);
hepatic fibrosis;
transforming growth factor beta 1 (TGF-β1);
COL1α2;
MMP-2;
TIMP-1;
Smad 2/3
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
2017;38(6):857-861
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of all-trans retinioc acid (ATRA)on proliferation of rat hepatic stellate cells (HSC-T6)and expressions of collagen Ⅰ,matrix metalloproteinase-2 (MMP-2),tissue inhibitor of metalloproteinases-1 (TIMP-1 )and signal protein Smad2/3 in TGF-β1-simulated HSC-T6 so as to explore the impact and molecular mechanisms of ATRA on liver fibrosis in vitro .Methods Cultured HSC-T6s were treated with different concentrations of ATRA (0.1,1,10 μmol/L)for fixed time (12,24,48 hours).After intervention time,cell proliferation was evaluated by MTT.Meanwhile,HSC-T6s stimulated by TGF-β1 (5 ng/mL)were treated with different concentrations of ATRA for 24 h.The mRNA expressions of COL1α2,MMP-2 and TIMP-1 were quantified by RT-PCR;the expression of Smad 2/3 protein was determined by cell immunochemistry.Results The proliferation of hepatic stellate cells was inhibited by ATRA in a dose-dependent manner (P < 0.05 ).After induced by TGF-β1,the mRNA expressions of COL1α2,MMP-2 and TIMP-1 and the expression of Smad 2/3 protein were increased significantly compared with control group (P <0.05).However,ATRA could obviously reduce themRNA expressions of COL1α2,MMP-2 and TIMP-1 and the expression of Smad 2/3 protein in HSC-T6 induced by TGF-β1 (P < 0.05 ).Conclusion ATRA can inhibit the proliferation of HSC-T6s and reduce the mRNA expressions of COL1α2,MMP-2 and TIMP-1 in HSC-T6 which were induced by TGF-β1.The anti-hepatic fibrosis function of ATRA may be related to its inhibition on the expression of Smad 2/3 protein in HSC-T6 to influence TGF-β1/Smad signaling pathway.
