PI3K/Akt signaling is involved in the pathogenesis of bleomycin‑induced pulmonary fibrosis via regulation of epithelial‑mesenchymal transition

  • Authors:
    • Xiao‑Ling Zhang
    • Rong‑Ge Xing
    • Liang Chen
    • Chun‑Rong Liu
    • Zhi‑Gang Miao
  • View Affiliations

  • Published online on: November 22, 2016     https://doi.org/10.3892/mmr.2016.5960
  • Pages: 5699-5706
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by chronic inflammation, fibroblast proliferation and extracellular matrix deposition. However, the molecular and cellular mechanisms underlying the pathogenesis of pulmonary fibrosis remain to be fully elucidated. The contribution of the phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt) pathway in fibrotic processes remains to be investigated. The aim of the present study was to investigate the role of the PI3K/Akt pathway in pulmonary fibrosis. A rat model of pulmonary fibrosis was induced by intratracheal administration of bleomycin (BLM), and a specific PI3K/Akt inhibitor, LY294002, was used to assess the role of the PI3K/Akt pathway in fibrogenesis. The inflammatory and fibrotic alterations in the lung tissues were evaluated using histological staining and the hydroxyproline assay. In addition, the concentration of cytokines in bronchoalveolar lavage fluid and the expression of Akt, phosphorylated (p‑)Akt, epithelial cadherin, α smooth muscle actin and vimentin in lung tissues. The data demonstrated that an increase in the expression levels of p‑Akt was involved in the progression of pulmonary fibrosis and contributed to fibrogenesis. Administration of the Akt inhibitor significantly attenuated inflammation and fibrosis, which was accompanied by a reversal of lung fibrosis‑associated epithelial‑mesenchymal transition. Taken together, these observations suggest that the PI3K/Akt pathway serves a central role in the pathophysiology of lung fibrosis, and is a promising therapeutic target.
View Figures
View References

Related Articles

Journal Cover

December-2016
Volume 14 Issue 6

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang XL, Xing RG, Chen L, Liu CR and Miao ZG: PI3K/Akt signaling is involved in the pathogenesis of bleomycin‑induced pulmonary fibrosis via regulation of epithelial‑mesenchymal transition. Mol Med Rep 14: 5699-5706, 2016
APA
Zhang, X., Xing, R., Chen, L., Liu, C., & Miao, Z. (2016). PI3K/Akt signaling is involved in the pathogenesis of bleomycin‑induced pulmonary fibrosis via regulation of epithelial‑mesenchymal transition. Molecular Medicine Reports, 14, 5699-5706. https://doi.org/10.3892/mmr.2016.5960
MLA
Zhang, X., Xing, R., Chen, L., Liu, C., Miao, Z."PI3K/Akt signaling is involved in the pathogenesis of bleomycin‑induced pulmonary fibrosis via regulation of epithelial‑mesenchymal transition". Molecular Medicine Reports 14.6 (2016): 5699-5706.
Chicago
Zhang, X., Xing, R., Chen, L., Liu, C., Miao, Z."PI3K/Akt signaling is involved in the pathogenesis of bleomycin‑induced pulmonary fibrosis via regulation of epithelial‑mesenchymal transition". Molecular Medicine Reports 14, no. 6 (2016): 5699-5706. https://doi.org/10.3892/mmr.2016.5960