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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 / Copyright

    Affiliations: Laboratory of Disease Model Research Center, College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang 163319, P.R. China, Department of Library and Information Center, Library of Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang 163319, P.R. China, School of Life Sciences, KUN Creative Bioresearch Group, Kyungpook National University, Daegu, Gyeongsangbuk 702‑701, Republic of Korea, Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology, Ibam‑myeon, Jeongeup‑si, Jeonbuk 56216, Republic of Korea
    Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1831-1838
    |
    Published online on: June 26, 2020
       https://doi.org/10.3892/mmr.2020.11279
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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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Copy and paste a formatted citation
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
Copy and paste a formatted citation
x
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
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