Study the role of lysosome-associated membrane protein type 2A for immune-mediated liver injury of primary biliary cholangitis
10.3760/cma.j.issn.1007-3418.2018.11.008
- VernacularTitle: 溶酶体相关膜蛋白2A在原发性胆汁性胆管炎肝脏免疫损伤中的作用
- Author:
Lu WANG
1
;
Miao ZHANG
;
Keshuai SUN
;
Xia ZHOU
;
Ying HAN
Author Information
1. Department of Digestive Disease, Xijing Hospital, the Military Medical University of Air Force PLA, Xi'an 710032, China
- Publication Type:Journal Article
- Keywords:
Primary biliary cholangitis;
Lysosome-associated membrane glycoprotein 2;
Chaperone-mediated autophagy;
Immune injury
- From:
Chinese Journal of Hepatology
2018;26(11):847-851
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of lysosome-associated membrane protein type 2A (LAMP-2A) for immune-mediated liver injury of primary biliary cholangitis (PBC).
Methods:The association between LAMP-2A expression and PBC was examined by immunohistochemistry and electron microscopy in liver tissue samples from patients with PBC. Furthermore, the immunological damage of LAMP-2A overexpression on mouse liver was observed by adeno-associated virus (AAV) overexpression technique. The expression level of mRNA was analyzed by Student's t-test. The data were graphed and analyzed statistically using graphpad prism 5 (GraphPad Software).A value of p < 0.05 was considered statistically significant.
Results:The expression of LAMP-2A in liver tissue of PBC patients was increased, and the autophagosome formation was observed in hepatocytes. C57BL/6 mice were injected into the caudal vein with LAMP-2A AAV for 6 weeks. The formation of autophagosomes in mouse hepatocytes was increased significantly. The expression of related molecules was abnormal; simultaneously, the degree of lymphocyte infiltration in the liver tissue of mice was significantly higher than the control group.
Conclusion:An overexpression of LAMP-2A in the liver of patients with PBC may induce and/or promote the hepatic inflammatory response, especially the portal inflammatory infiltrate.