| First Author | Ji YR | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 452 |
| Issue | 3 | Pages | 822-7 |
| PubMed ID | 25201726 | Mgi Jnum | J:220094 |
| Mgi Id | MGI:5632231 | Doi | 10.1016/j.bbrc.2014.09.001 |
| Citation | Ji YR, et al. (2014) Over-expression of Roquin aggravates T cell mediated hepatitis in transgenic mice using T cell specific promoter. Biochem Biophys Res Commun 452(3):822-7 |
| abstractText | Chronic hepatitis is a major cause of liver cancer, so earlier treatment of hepatitis might be reducing liver cancer incidence. Hepatitis can be induced in mice by treatment with Concanavalin A (Con A); the resulting liver injury causes significant CD4(+) T cell activation and infiltration. In these T cells, Roquin, a ring-type E3 ubiquitin ligase, is activated. To investigate the role of Roquin, we examined Con A-induced liver injury and T cell infiltration in transgenic (Tg) mice overexpressing Roquin specifically in T cells. In Roquin Tg mice, Con A treatment caused greater increases in both the levels of liver injury enzymes and liver tissue apoptosis, as revealed by TUNEL and H&E staining, than wild type (WT) mice. Further, Roquin Tg mice respond to Con A treatment with greater increases in the T cell population, particularly Th17 cells, though Treg cell counts are lower. Roquin overexpression also enhances increases in pro-inflammatory cytokines, including IFN-gamma, TNF-alpha and IL-6, upon liver injury. Furthermore, Roquin regulates the immune response and apoptosis in Con A induced hepatitis via STATs, Bax and Bcl2. These findings suggest that over-expression of Roquin exacerbates T-cell mediated hepatitis. |
