Open Access

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

  • Authors:
    • 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
  • View Affiliations

  • Published online on: June 26, 2020     https://doi.org/10.3892/mmr.2020.11279
  • Pages: 1831-1838
  • Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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 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 wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 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.
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September-2020
Volume 22 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Jin MH, Shen GN, Jin YH, Sun HN, Zhen X, Zhang YQ, Lee DS, Cui YD, Yu LY, Kim JS, Kim JS, et al: Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway. Mol Med Rep 22: 1831-1838, 2020
APA
Jin, M., Shen, G., Jin, Y., Sun, H., Zhen, X., Zhang, Y. ... Han, Y. (2020). Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway. Molecular Medicine Reports, 22, 1831-1838. https://doi.org/10.3892/mmr.2020.11279
MLA
Jin, M., Shen, G., Jin, Y., Sun, H., Zhen, X., Zhang, Y., Lee, D., Cui, Y., Yu, L., Kim, J., Kwon, T., Han, Y."Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway". Molecular Medicine Reports 22.3 (2020): 1831-1838.
Chicago
Jin, M., Shen, G., Jin, Y., Sun, H., Zhen, X., Zhang, Y., Lee, D., Cui, Y., Yu, L., Kim, J., Kwon, T., Han, Y."Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway". Molecular Medicine Reports 22, no. 3 (2020): 1831-1838. https://doi.org/10.3892/mmr.2020.11279