Title:Explore on the Mechanism of miRNA-146a/TAB1 in the Regulation
of Cellular Apoptosis and Inflammation in Ulcerative Colitis Based
on NF-κB Pathway
Volume: 24
Author(s): Xiaoying Xia, Qian Yang, Xue Han, Yulin Du, Shujun Guo, Mengqing Hua, Fang Fang, Zhigang Ma, Hua Ma, Hui Yuan, Wenjing Tian, Zebang Ding, Yanan Duan, Qi Huo and Yao Li*
Affiliation:
- Anhui Provincial Key Laboratory of Immunology in Chronic Diseases, Anhui Provincial Key Laboratory of
Infection and Immunology, Department of Immunology, School of Laboratory Medicine, Bengbu Medical
College, Bengbu 233030, China
Keywords:
ulcerative colitis;, miR-146a;, TAB1;, apoptosis;, inflammation
Abstract: Objective: Ulcerative colitis (UC) is a chronic non-specific inflammatory
disease of the rectum and colon with unknown etiology. A growing number of evidence
suggest that the pathogenesis of UC is related to excessive apoptosis and production
of inflammatory cytokines. However, the functions and molecular mechanisms
associated with UC remain unclear.
Materials and Methods: The in vivo and in vitro models of UC were established in this
study. MiRNA or gene expression was measured by qRT-PCR assay. ELISA, CCK-8,
TUNEL, and flow cytometry assays were applied for analyzing cellular functions. The
interactions between miR-146a and TAB1 were verified by luciferase reporter and
miRNA pull-down assays.
Results: MiR-146a was obviously increased in UC patients, DSS-induced colitis mice,
and TNF-ɑ-induced YAMC cells, when compared to the corresponding controls. MiR-
146a knockdown inhibited the inflammatory response and apoptosis in DSS-induced
colitis mice and TNF-ɑ-induced YAMC cells. Mechanistically, we found that TAB1 was
the target of miR-146a and miR-146a knockdown suppressed the activation of NF-κB
pathway in UC. More importantly, TAB1 could overturn the inhibitory effect of
antagomiR-146a on cell apoptosis and inflammation in UC.
Conclusion: MiR-146a knockdown inhibited cell apoptosis and inflammation via
targeting TAB1 and suppressing NF-κB pathway, suggesting that miR-146a may be a
new therapeutic target for UC treatment.
