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Biomed Pharmacother. 2017 May;89:1387-1391. doi: 10.1016/j.biopha.2017.03.021. Epub 2017 Mar 19.

CTRP3 attenuates hepatic stellate cell activation through transforming growth factor-β/Smad signaling pathway.

Author information

1
Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
2
Department of Thoracic Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
3
Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China. Electronic address: caogang_xa@126.com.
4
Department of Nephrology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China. Electronic address: xieli_yi@126.com.

Abstract

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.

KEYWORDS:

C1q/tumor necrosis factor-related protein 3; Extracellular matrix (ECM); Hepatic stellate cells (HSCs); Liver fibrosis

PMID:
28320106
DOI:
10.1016/j.biopha.2017.03.021
[Indexed for MEDLINE]

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