Effect of Low Expression of Vitamin D Receptor on Immune Response in Patients With Primary Biliary Cholangitis
10.3969/j.issn.1008-7125.2019.01.005
- Author:
Hui XIAO
1
Author Information
1. Department of Gastroenterology, Shangluo Central Hospital
- Publication Type:Journal Article
- Keywords:
Immune Response;
MiR-155;
Primary Biliary Cholangitis;
SOCS-1;
Vitamin D Receptor
- From:
Chinese Journal of Gastroenterology
2019;24(1):21-24
- CountryChina
- Language:Chinese
-
Abstract:
Background: Immune function plays a key role in the development of primary biliary cholangitis (PBC). Vitamin D plays an immunomodulatory role through vitamin D receptor (VDR) and may participate in the development and progression of PBC. Aims: To investigate the effect of low expression of VDR on immune response in patients with PBC. Methods: Thirty patients with PBC were enrolled, and 30 patients with non-PBC were served as controls. mRNA expressions of VDR, SOCS-1, miR-155 in liver tissue and peripheral blood mononuclear cell (PBMC) were detected by real-time quantitative PCR, protein expressions of VDR, SOCS-1 were measured by Western blotting and immunohistochemistry. Expressions of VDR, SOCS-1 and miR-155 in liver tissue and PBMC were compared between PBC group and control group. Correlations of expressions of VDR, SOCS-1 and miR-155 in liver tissue in patients with PBC were analyzed. Results: Compared with control group, mRNA and protein expressions of VDR and SOCS-1 were significantly decreased (P<0.05), and expression of miR-155 in liver tissue was significantly increased in PBC patients (P<0.05). The mRNA and protein expressions of VDR and SOCS-1 in PBMC were significantly decreased in PBC group than in control group (P<0.05). There was a significant positive correlation between VDR protein and SOCS-1 expression and a negative correlation between expressions of miR-155 and VDR, SOCS-1 in liver tissue of PBC patients. Conclusions: The expression of VDR in patients with PBC is significantly decreased. VDR may be involved in the regulation of development and progression of PBC through miR-155 and SOCS-1.
