| First Author | Jin MH | Year | 2020 |
| Journal | Mol Med Rep | Volume | 22 |
| Issue | 3 | Pages | 1831-1838 |
| PubMed ID | 32705184 | Mgi Jnum | J:294848 |
| Mgi Id | MGI:6458855 | Doi | 10.3892/mmr.2020.11279 |
| Citation | Jin MH, et al. (2020) Peroxiredoxin I deficiency increases pancreatic betacell apoptosis after streptozotocin stimulation via the AKT/GSK3beta signaling pathway. Mol Med Rep 22(3):1831-1838 |
| abstractText | Apoptosis of pancreatic betacells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic betacell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)induced apoptosis of pancreatic betacells was investigated. The expression level of Prx I was decreased by STZ treatment in a timedependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wildtype and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)3beta phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated betacatenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZinduced pancreatic betacell death in vivo and in vitro by regulating the AKT/GSK3beta/betacatenin signaling pathway, as well as NFkappaB signaling. These findings provide a theoretical basis for treatment of pancreatic damage. |
