The Journal of Practical Medicine ›› 2023, Vol. 39 ›› Issue (17): 2176-2182.doi: 10.3969/j.issn.1006-5725.2023.17.005

• Basic Research • Previous Articles     Next Articles

Preliminary study on the mechanism of TMEM39A in primary biliary cholangitis

Xiaotong SUN1,Chongxu HAN1,2(),Chan WANG1,Chuanli REN2,Mingming. ZHANG3   

  1. Medical College of Yangzhou University,Yangzhou 225009,China
  • Received:2023-03-27 Online:2023-09-10 Published:2023-09-27
  • Contact: Chongxu HAN E-mail:hanchongxu@126.com

Abstract:

Objective To explore the mechanism of TMEM39A in primary biliary cholangitis. Method In order to study how TMEM39A regulates the expression of autophagy in primary biliary cholangitis, human hepatobiliary cancer cell RBE was selected for study. Human hepatobiliary cancer cells were treated with the hydrophobic bile acid glycine deoxycholic acid (GCDC) into three groups: control group, 500 μmol/L group and 1 000 μmol/L group. Cell counting kits (CCK-8), cell cloning, cell scratching, and Hoechst staining assays were used to detect cell viability, proliferation, wound healing rates, and apoptosis. qPCR detected TMEM39A mRNA expression in cells; Western Blot detects protein expression of TMEM39A and LC3. Results Compared with control group, cell viability, proliferation and wound healing rate were decreased in 1 000 μmol/L group, while apoptosis was the most obvious. In the constructed model of primary biliary cholangitis, overexpression of TMEM39A promoted LC3 expression. Conclusion The increased expression of TMEM39A leads to enhanced autophagy of bile duct cells and bile duct damage, which may be one of the mechanisms causing primary biliary cholangitis.

Key words: TMEM39A, primary biliary cholangitis, human hepatobiliary duct cancer cells, LC3, glycochenodeoxycholic acid

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