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Article

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

  • Authors:
    • Minghui Jia
    • Xiaoyun Chen
    • Jili Liu
    • Jun Chen
  • View Affiliations / Copyright

    Affiliations: Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
  • Pages: 571-579
    |
    Published online on: October 26, 2017
       https://doi.org/10.3892/mmr.2017.7912
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Abstract

Chronic rhinosinusitis (CRS) is a form of chronic inflammation of the nasal cavity and paranasal sinus with multi‑causal pathogenesis, including oxidative stress. Several lines of evidence have demonstrated that the phosphatase and tensin homolog gene (PTEN) can inhibit the activation of phosphoinositide 3‑kinase (PI3K) to affect phosphorylation of Akt. Importantly, the PI3K/PTEN/Akt signaling pathway is associated with various types of tumors, chronic inflammatory diseases, and autoimmune disease through its regulation of cell growth, apoptosis, proliferation, and metabolism. This in vitro study aimed to investigate the role of PTEN and the relationship between PTEN and the PI3K/Akt pathway in nasal epithelial cells under oxidative stress. H2O2 treatment was applied to induce a cell injury model of oxidative stress in rat nasal epithelial cells. Cells were divided into control, H2O2, H2O2+PTEN, and H2O2+siPTEN groups. Cell viability was measured using the CCK‑8 assay, and reactive oxygen species (ROS) levels and apoptosis rates were analyzed by flow cytometry (FCM). Oxidative parameters, including ROS, catalase (CAT), and malondialdehyde (MDA), were tested by enzyme‑linked immunosorbent assay (ELISA). The expression of apoptosis‑related genes and PI3K/Akt pathway was assayed by quantitative PCR (qPCR) and western blot. In H2O2‑injured cells, oxidative stress, due to increased ROS levels and apoptosis rates, was induced, and PTEN aggravated the injury. The levels of both p‑Akt and PTEN in H2O2‑injured cells were positively correlated and higher than in control cells. Unknown regulatory protein(s) may exist in the PI3K/PTEN/Akt pathway or the PTEN and PI3K/Akt pathways may be two independent signaling pathways that have cross interactions.
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Copy and paste a formatted citation
Spandidos Publications style
Jia M, Chen X, Liu J and Chen J: PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways. Mol Med Rep 17: 571-579, 2018.
APA
Jia, M., Chen, X., Liu, J., & Chen, J. (2018). PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways. Molecular Medicine Reports, 17, 571-579. https://doi.org/10.3892/mmr.2017.7912
MLA
Jia, M., Chen, X., Liu, J., Chen, J."PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways". Molecular Medicine Reports 17.1 (2018): 571-579.
Chicago
Jia, M., Chen, X., Liu, J., Chen, J."PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways". Molecular Medicine Reports 17, no. 1 (2018): 571-579. https://doi.org/10.3892/mmr.2017.7912
Copy and paste a formatted citation
x
Spandidos Publications style
Jia M, Chen X, Liu J and Chen J: PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways. Mol Med Rep 17: 571-579, 2018.
APA
Jia, M., Chen, X., Liu, J., & Chen, J. (2018). PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways. Molecular Medicine Reports, 17, 571-579. https://doi.org/10.3892/mmr.2017.7912
MLA
Jia, M., Chen, X., Liu, J., Chen, J."PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways". Molecular Medicine Reports 17.1 (2018): 571-579.
Chicago
Jia, M., Chen, X., Liu, J., Chen, J."PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways". Molecular Medicine Reports 17, no. 1 (2018): 571-579. https://doi.org/10.3892/mmr.2017.7912
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