The Role of miR‐497/EIF3A Axis in TGFβ1‐Induced Epithelial–Mesenchymal Transition and Extracellular Matrix in Rat Alveolar Epithelial Cells and Pulmonary Fibroblasts. Issue 10 (3rd May 2017)

• Record Type: Journal Article
• Authors: Guo, Ren; Lv, Yu; Ouyang, Yang; Liu, Siyu; Li, Dai
• Is Part Of: Journal of cellular biochemistry. Volume 118:Issue 10(2017)
• Page Start: 3401
• Page End: 3408
• Publication Date: 2017-05-03
• Subjects: EIF3A -- TGFβ1 -- EPITHELIAL–MESENCHYMAL TRANSITION -- miR‐497 -- PULMONARY FIBROSIS -- ALVEOLAR EPITHELIAL CELL; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.25997
• Languages: English
• ISSNs: 0730-2312

Abstract

ABSTRACT: Multi‐cause‐induced interstitial lung disease, particularly pulmonary fibrosis, is a serious clinical concern. Fibroblasts have been suggested to have a major role, with it recently being revealed that some of these fibroblasts are derived from alveolar epithelial cells through epithelial–mesenchymal transition (EMT). Eukaryotic translation initiation factor 3 subunit A (EIF3A) is a protein that in humans is encoded by the EIF3A gene, and has been suggested to play roles in regulating translation of a subset of mRNAs and in regulating cell cycle progression and cell proliferation. In the present study, we chose a well‐known TGFβ1‐induced EMT model in alveolar epithelial cells to investigate the functional role of EIF3A. TGFβ1‐induced EIF3A expression and EMT process in alveolar epithelial cells, after EIF3A knockdown, the EMT process could be partially reversed. Online tools and luciferase assays showed that miR‐497 could inhibit EIF3A expression by directly binding to the 3′UTR of EIF3A. Ectopic miR‐497 expression partially reversed TGFβ1‐induced EMT in alveolar epithelial cells. In addition, miR‐497 could suppress TGFβ1‐induced pulmonary fibroblast proliferation and EIF3A, Collagen I and α‐SMA protein levels. Taken together, EIF3A could promote TGFβ1‐induced EMT in alveolar epithelial cells; miR‐497 suppressed TGFβ1‐induced EMT in alveolar epithelial cells TGFβ1‐induced excessive proliferation and ECM in pulmonary fibroblast through inhibiting EIF3A by targeting. MiR‐497/EIF3A axis shows the potential to be effective in the treatment of pulmonary fibrosis. J. Cell. Biochem. 118: 3401–3408, 2017. © 2017 Wiley Periodicals, Inc. Abstract : EIF3A could promote TGFβ1‐induced EMT in alveolar epithelial cells; miR‐497 suppressed TGFβ1‐induced EMT in alveolar epithelial cells and TGFβ1‐induced excessive proliferation and ECM in fibroblast through inhibiting EIF3A by targeting. MiR‐497/EIF3A axis shows the potential to be effective in the treatment of pulmonary fibrosis.