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CD147 Promotes CXCL1 Expression and Modulates Liver Fibrogenesis
Wen-Pu Shi1, Di Ju2, Hao Li3
1Department of Cell Biology, National Translational Science Center for Molecular Medicine, State Key Laboratory of Cancer Biology, Fourth Military Medical University, Xi'an 710032, China. shiwenpu126@163.com.
International Journal of Molecular Sciences
|April 13, 2018
Summary
Targeting CD147 may treat liver fibrosis. CD147 activates hepatic stellate cells (HSCs) and upregulates CXCL1, promoting liver fibrosis. Inhibiting CD147 reduces fibrosis and inflammation.
Area of Science:
- Hepatology
- Cell Biology
- Immunology
Background:
- Activated hepatic stellate cells (HSCs) drive liver fibrosis through inflammatory and fibrogenic factor release.
- CXC chemokine-ligand-1 (CXCL1) is expressed on HSCs, and CD147 is overexpressed in activated HSCs.
Purpose of the Study:
- To investigate the role of CD147 in promoting liver fibrosis by activating HSCs and regulating chemokine expression.
- To explore the therapeutic potential of targeting CD147 for liver fibrosis.
Main Methods:
- Utilized mice with CD147 specific deletion in HSCs to assess CCl₄-induced liver fibrosis.
- Investigated the effect of CD147 overexpression on CXCL1 secretion.
- Examined the role of CXCL1 in HSC activation via autocrine signaling.
- Assessed the impact of PI3K/AKT inhibitor on CD147-induced CXCL1 expression.
Main Results:
- CD147 specific deletion in HSCs alleviated CCl₄-induced liver fibrosis and inhibited HSC activation.
- Overexpression of CD147 upregulated CXCL1 secretion, which promoted HSC activation through autocrine signaling.
- PI3K/AKT inhibitor treatment suppressed CD147-induced CXCL1 expression, indicating CD147 regulates CXCL1 via PI3K/AKT signaling.
Conclusions:
- CD147 plays a crucial role in liver fibrosis by activating HSCs and regulating CXCL1 release through the PI3K/AKT pathway.
- Inhibition of CD147 attenuates CCl₄-induced liver fibrosis and inflammation.
- Targeting CD147 represents a promising therapeutic strategy for liver fibrosis.
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