Open Access

Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway

  • Authors:
    • Wei‑Na Duan
    • Zhong‑Yuan Xia
    • Min Liu
    • Qian Sun
    • Shao‑Qing Lei
    • Xiao‑Jing Wu
    • Qing‑Tao Meng
    • Yan Leng
  • View Affiliations

  • Published online on: July 6, 2017     https://doi.org/10.3892/mmr.2017.6941
  • Pages: 2668-2674
  • Copyright: © Duan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have suggested that the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway is involved in hyperglycemia‑induced lung injury. The present study aimed to investigate the roles of suppressor of cytokine signaling3 (SOCS3) in the regulation of JAK2/STAT3 activation following high glucose (HG) treatment in A549 human pulmonary epithelial cells. Cell viability was evaluated using Cell Counting Kit-8 and lactate dehydrogenase assays. HG‑induced inflammatory injury in A549 cells was assessed through the evaluation of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) levels using ELISA. The protein expression levels of SOCS3, JAK2, STAT3, phosphorylated (p)‑JAK2 and p‑STAT3 were determined using western blot analysis. Cellular viability was significantly decreased, whereas IL‑6 and TNF‑α levels were significantly increased, following HG stimulation of A549 cells. In addition, the protein levels of SOCS3, p‑JAK2 and p‑STAT3 were significantly increased in HG‑treated cells. Treatment with the JAK2/STAT3 inhibitor tyrphostin AG490, or SOCS3 overexpression, appeared to prevent the HG‑induced alterations in protein expression. Furthermore, cellular viability was enhanced, whereas the levels of proinflammatory cytokines were suppressed. These finding suggested the involvement of the SOCS3/JAK2/STAT3 signaling pathway in HG‑induced responses in lung cells. Therefore, it may be hypothesized that the inhibition of the JAK2/STAT3 pathway through SOCS3 overexpression may prevent hyperglycemia‑induced lung injury, and may have therapeutic potential for the treatment of patients with diabetic lung injury.
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September-2017
Volume 16 Issue 3

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

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Spandidos Publications style
Duan WN, Xia ZY, Liu M, Sun Q, Lei SQ, Wu XJ, Meng QT and Leng Y: Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway. Mol Med Rep 16: 2668-2674, 2017
APA
Duan, W., Xia, Z., Liu, M., Sun, Q., Lei, S., Wu, X. ... Leng, Y. (2017). Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway. Molecular Medicine Reports, 16, 2668-2674. https://doi.org/10.3892/mmr.2017.6941
MLA
Duan, W., Xia, Z., Liu, M., Sun, Q., Lei, S., Wu, X., Meng, Q., Leng, Y."Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway". Molecular Medicine Reports 16.3 (2017): 2668-2674.
Chicago
Duan, W., Xia, Z., Liu, M., Sun, Q., Lei, S., Wu, X., Meng, Q., Leng, Y."Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway". Molecular Medicine Reports 16, no. 3 (2017): 2668-2674. https://doi.org/10.3892/mmr.2017.6941