| First Author | Zhang M | Year | 2021 |
| Journal | Int Immunopharmacol | Volume | 101 |
| Issue | Pt B | Pages | 108318 |
| PubMed ID | 34775365 | Mgi Jnum | J:357958 |
| Mgi Id | MGI:6857515 | Doi | 10.1016/j.intimp.2021.108318 |
| Citation | Zhang M, et al. (2021) MicroRNA-497 inhibits inflammation in DSS-induced IBD model mice and lipopolysaccharide-induced RAW264.7 cells via Wnt/beta-catenin pathway. Int Immunopharmacol 101(Pt B):108318 |
| abstractText | BACKGROUND AND AIMS: MicroRNA (miR)-497 is downregulated in several inflammatory diseases, excluding inflammatory bowel disease (IBD). The aim of this study is to evaluate whether miR-497 inhibits gut inflammation both in vivo and in vitro. METHODS: The 3% dextran sulphate sodium (DSS) was used to induce experimental colitis, while 1 mug/ml lipopolysaccharide (LPS) was for RAW264.7 cell damage.Colitis severity was evaluated by disease activity index (DAI), colon length, histopathologic injury, etc. The nuclear transcription factor NF-kappaB activity in colon tissues was also estimated by western blot. Then, the quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate the expression levels of miR-497, pro-inflammatory cytokines and chemokines in colon tissues and RAW264.7 cells. Furthermore, the activity of Wnt/beta-catenin pathway was determined by western blot and TOP/FOP-flash reporter assays. RESULTS: The level of miR-497 was reduced in inflamed mucosa from IBD patients, mice with colitis and LPS-treated RAW264.7 cells. miR-497 knockout (miR-497 KO) mice were more susceptible to DSS-induced colitis, with increased inflammatory response, compared with control mice. Furthermore, the overexpression of miR-497 reduced the release of pro-inflammatory cytokines and chemokines in LPS-treated RAW264.7 cells. Finally, we found that miR-497 inhibited inflammation through Wnt/beta-catenin pathway both in vitro and in vivo. CONCLUSION: Our data indicate that miR-497 inhibits inflammation in DSS-induced IBD model mice and LPS-induced RAW264.7 cells by inhibiting the activation of NF-kappaB pathway and the release of cytokines, indicating that miR-497 plays a key role in the progression of IBD. Thus, therapeutic regulation of miR-497 expression may be beneficial for the treatment of IBD. |
