Involvement of TLR2-MyD88 in abnormal expression of miR-146a in peripheral blood monocytes of patients with chronic hepatitis C.
10.1007/s11596-015-1414-5
- Author:
Wen-jing ZHANG
1
;
Hua WANG
;
Qiao-xia TONG
;
Sheng-hua JIE
;
Dong-liang YANG
;
Cheng PENG
Author Information
1. Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China, 309578577@qq.com.
- Publication Type:Journal Article
- MeSH:
Adult;
Base Sequence;
Cell Line;
DNA Primers;
Female;
Hepatitis C, Chronic;
blood;
Humans;
Male;
MicroRNAs;
blood;
Middle Aged;
Monocytes;
metabolism;
Myeloid Differentiation Factor 88;
physiology;
Reverse Transcriptase Polymerase Chain Reaction;
Toll-Like Receptor 2;
physiology;
Young Adult
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(2):219-224
- CountryChina
- Language:English
-
Abstract:
miR-146a is an immunoregulatory microRNA closely associated with viral infection. This study investigated the expression changes of miR-146a in peripheral blood monocytes of HCV-infected patients and the mechanism by which the THP-1 cells were stimulated with HCV core protein in vitro. It was found that in the peripheral blood monocytes of HCV-infected patients, miR-146a expression was upregulated. After treated by interferon/ribavirin, miR-146a expression was decreased when HCV RNA became undetectable. HCV core could directly stimulate THP-1 cells to produce miR-146a. Silencing TLR2 and MyD88 could significantly inhibit the expression of miR-146a. It was concluded that the expression of miR-146a in peripheral blood monocytes of HCV-infected patients was abnormally increased. The TLR2-MyD88 signaling pathway may take part in the overexpression of miR-146a in monocytes stimulated with HCV core protein.
