| First Author | Mori H | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 359 |
| Issue | 4 | Pages | 952-8 |
| PubMed ID | 17562326 | Mgi Jnum | J:122729 |
| Mgi Id | MGI:3715377 | Doi | 10.1016/j.bbrc.2007.05.198 |
| Citation | Mori H, et al. (2007) Suppression of SOCS3 expression in the pancreatic beta-cell leads to resistance to type 1 diabetes. Biochem Biophys Res Commun 359(4):952-8 |
| abstractText | Type 1 diabetes results from the selective destruction of insulin-producing pancreatic beta-cells during islet inflammation, which involves inflammatory cytokines and free radicals. However, mechanisms for protecting beta-cells from destruction have not been clarified. In this study, we define the role of SOCS3 on beta-cell destruction using beta-cell-specific SOCS3-conditional knockout (cKO) mice. The beta-cell-specific SOCS3-deficient mice were resistant to the development of diabetes caused by streptozotocin (STZ), a genotoxic methylating agent, which has been used to trigger beta-cell destruction. The islets from cKO mice demonstrated hyperactivation of STAT3 and higher induction of Bcl-xL than did islets from WT mice, and SOCS3-deficient beta-cells were more resistant to apoptosis induced by STZ in vitro than were WT beta-cells. These results suggest that enhanced STAT3 signaling protects beta-cells from destruction induced by a genotoxic stress and that STAT3/SOCS3 can be a potential therapeutic target for the treatment of type 1 diabetes. |
