Peroxiredoxin I deficiency increases pancreatic β-cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway

Mei Hua Jin, Gui Nan Shen, Ying Hua Jin, Hu Nan Sun, Xing Zhen, Yong Qing Zhang, Dong Seok Lee, Yu Dong Cui, Li Yun Yu, Ji Su Kim, Taeho Kwon, Ying Hao Han

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Apoptosis of pancreatic β-cells 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 β-cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)-induced apoptosis of pancreatic β-cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time-dependent manner, and apoptosis of Prx I knockdown MIN 6 cells was increased by STZ stimulation, compared with untransduced MIN 6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild-type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)-3β phosphorylation significantly decreased following Prx I knockdown in MIN 6 cells. However, phosphorylated β-catenin 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 STZ-induced pancreatic β-cell death in vivo and in vitro by regulating the AKT/GSK-3β/β-catenin signaling pathway, as well as NF-κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.

Original languageEnglish
Pages (from-to)1831-1838
Number of pages8
JournalMolecular Medicine Reports
Volume22
Issue number3
DOIs
StatePublished - Sep 2020

Keywords

  • Apoptosis
  • Glycogen synthase kinase-3β signaling
  • Peroxiredoxin I
  • Streptozotocin
  • β-cell

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