| First Author | Jia X | Year | 2018 |
| Journal | Scand J Immunol | Volume | 88 |
| Issue | 3 | Pages | e12703 |
| PubMed ID | 30047999 | Mgi Jnum | J:357998 |
| Mgi Id | MGI:6881300 | Doi | 10.1111/sji.12703 |
| Citation | Jia X, et al. (2018) Increased M1 macrophages in young miR-15a/16(-/-) mice with tumour grafts or dextran sulphate sodium-induced colitis. Scand J Immunol 88(3):e12703 |
| abstractText | M1 macrophages are involved in inflammation by producing proinflammatory cytokines, whereas M2 macrophages are associated with wound healing and tissue regeneration by producing anti-inflammatory cytokines. MicroRNAs are involved in macrophage polarization. To evaluate whether miR-15a/16 is involved in macrophage polarization under tumour or inflammation microenvironments, we observed the growth of transplanted hepatic cancer (H22) cells or severity of dextran sulphate sodium (DSS)-induced colitis in 8-week-old miR-15a/16 knockout (KO) mice. Compared with littermate controls, the miR-15a/16(-/-) mice exhibited retarded tumour growth and increased sensibility to DSS-induced colitis. Meanwhile, the M1 cell frequencies were higher in tumour tissues and inflamed colons of KO mice than of littermate controls. Macrophages with miR-15a/16 deletion revealed an enhanced NF-kappaB transcription under the physiological state and lipopolysaccharide (LPS) or high mobility group box 1 (HMGB1) stimulation. STAT3 expression was also significantly increased in miR-15a/16(-/-) macrophages under LPS or HMGB1 stimulation. The polarization of M1 macrophages can be associated with the coactivation of NF-kappaB and STAT3. Results indicated that miR-15a/16 deficiency in the macrophages directs M1 polarization for tumour suppression and proinflammation. Thus, miR-15a/16 deletion in macrophages holds a distinct biological significance from that of the microRNA deficiency in tumour cells. |
