TY - JOUR
T1 - CTRP3 attenuates hepatic stellate cell activation through transforming growth factor-β/Smad signaling pathway
AU - Cheng, Chuantao
AU - Yu, Shuo
AU - Kong, Ran
AU - Yuan, Qinggong
AU - Ma, Yuefeng
AU - Yang, Wenbin
AU - Cao, Gang
AU - Xie, Liyi
N1 - Publisher Copyright:
© 2017 Elsevier Masson SAS
PY - 2017/5/1
Y1 - 2017/5/1
N2 - Activation of hepatic stellate cells (HSCs) plays a pivotal role in the development of liver fibrosis. C1q/tumor necrosis factor-related protein 3 (CTRP3), a member of CTRPs, was involved in fibrosis. However, little is known about the role of CTRP3 in liver fibrosis. This study aimed to determine its role in liver fibrosis and explore the possible mechanism. Our results demonstrated that CTRP3 was lowly expressed in liver fibrosis tissues and activated HSCs. Overexpression of CTRP3 inhibited the proliferation and migration of HSCs, as well as suppressed the expression of extracellular matrix (ECM) in transforming growth factor-β1 (TGF-β1)-stimulated HSC-T6 cells. Furthermore, CTRP3 overexpression greatly inhibited the expression level of phosphorylation of Smad3 in TGF-β1-stimulated HSC-T6 cells. In conclusion, the present study demonstrated that CTRP3 inhibited the proliferation and migration of TGF-β1-induced HSC-T6 cells and attenuated liver fibrosis, at least in part, through inhibiting the Smad signaling pathway. These findings suggest that CTRP3 may be a promising therapeutic target for the treatment of liver fibrosis.
AB - Activation of hepatic stellate cells (HSCs) plays a pivotal role in the development of liver fibrosis. C1q/tumor necrosis factor-related protein 3 (CTRP3), a member of CTRPs, was involved in fibrosis. However, little is known about the role of CTRP3 in liver fibrosis. This study aimed to determine its role in liver fibrosis and explore the possible mechanism. Our results demonstrated that CTRP3 was lowly expressed in liver fibrosis tissues and activated HSCs. Overexpression of CTRP3 inhibited the proliferation and migration of HSCs, as well as suppressed the expression of extracellular matrix (ECM) in transforming growth factor-β1 (TGF-β1)-stimulated HSC-T6 cells. Furthermore, CTRP3 overexpression greatly inhibited the expression level of phosphorylation of Smad3 in TGF-β1-stimulated HSC-T6 cells. In conclusion, the present study demonstrated that CTRP3 inhibited the proliferation and migration of TGF-β1-induced HSC-T6 cells and attenuated liver fibrosis, at least in part, through inhibiting the Smad signaling pathway. These findings suggest that CTRP3 may be a promising therapeutic target for the treatment of liver fibrosis.
KW - C1q/tumor necrosis factor-related protein 3
KW - Extracellular matrix (ECM)
KW - Hepatic stellate cells (HSCs)
KW - Liver fibrosis
UR - https://www.scopus.com/pages/publications/85015450586
U2 - 10.1016/j.biopha.2017.03.021
DO - 10.1016/j.biopha.2017.03.021
M3 - 文章
C2 - 28320106
AN - SCOPUS:85015450586
SN - 0753-3322
VL - 89
SP - 1387
EP - 1391
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
ER -