| First Author | Zhang Q | Year | 2017 |
| Journal | Oncotarget | Volume | 8 |
| Issue | 39 | Pages | 65397-65406 |
| PubMed ID | 29029439 | Mgi Jnum | J:294318 |
| Mgi Id | MGI:6455679 | Doi | 10.18632/oncotarget.18541 |
| Citation | Zhang Q, et al. (2017) MicroRNA-149* suppresses hepatic inflammatory response through antagonizing STAT3 signaling pathway. Oncotarget 8(39):65397-65406 |
| abstractText | Chronic inflammation is increasingly recognized as an important component of tumorigenesis and metabolic diseases. The roles of microRNA149* (miRNA149*) in inflammation remain poorly understood. Here, we demonstrate that miR-149* is a suppressor of STAT3-mediated inflammation. MiR-149*-/- mice were generated with CRISPR/CAS9 technique. In a lipopolysaccharide (LPS)-induced inflammation model, miR-149*-/- mice show more severe liver injury and inflammation, compared with wild-type (WT) mice. MiR-149*-/- mice also displayed elevated messenger RNA (mRNA) levels of interleukin (IL)-6, inducible nitric oxide synthase (iNOS), complement C3 (C3) and IL-4 in response to LPS. Then miR-149* agomir administration is largely able to alleviate the LPS-induced some inflammatory gene expression in WT mouse liver. In vitro, miR-149* mimics inhibited expression of STAT3-meidated inflammatory mediators induced by LPS and suppresses the phosphorylation of STAT3 and its transcription activity in HepG2 cells. These findings identify miR-149* as a negative mediator of inflammation that may serve as an attractive therapeutic tool for immune and inflammatory liver diseases. |
