SLIT3 knockdown inhibited TGF-β-induced hepatic stellate cells activation by down-regulating YAP signal

被引:7
作者
Fu, Xiling [1 ]
Chang, Jiabao [1 ]
Jiao, Damin [1 ]
Zhu, Mengying [1 ]
Ma, Yuqi [1 ]
机构
[1] Nanjing Univ Chinese Med, Hosp Nanjing 2, Dept Hepatol, 1-1 Zhongfu Rd, Nanjing 210000, Jiangsu, Peoples R China
关键词
Liver fibrosis; Hepatic stellate cells; SLIT3; TGF-beta; YAP; LIVER FIBROSIS; DISEASES;
D O I
10.1007/s13273-023-00336-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Objective Liver fibrosis is a chronic liver disease caused by a variety of pathophysiological. However, there are no effective treatments to combat it. HSCs are a major source of fibrotic cells and exploring the mechanisms of HSC activation may provide new strategies for the treatment of liver fibrosis.Objectives To explore the role and underlying mechanism of SLIT3 in HSCs fibrosis.Results GSE163211 dataset analysis identified aberrant expression of SLIT3 in NASH F1-F4 tissues and SLIT3 expression level was positively correlated with fibrosis-related proteins. In vitro experiments showed that TGF-beta induced upregulation of SLIT3 in LX-2 cells. Knockdown of SLIT3 significantly inhibited TGF-beta-induced alpha-SMA, COL1A2, and COL1A1 expression, inhibited excessive cell proliferation and migration, and suppressed YAP activity.Conclusion Collectively, our findings suggest that SLIT3 deficiency alleviates TGF-beta-induced HSCs activation by inhibiting YAP activity.
引用
收藏
页码:251 / 258
页数:8
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