miR-205 Suppresses Pulmonary Fibrosis by Targeting GATA3 Through Inhibition of Endoplasmic Reticulum Stress

Author(s): Bingke Sun, Shumin Xu, Yanli Yan, Yusheng Li, Hongqiang Li, Guizhen Zheng, Tiancao Dong, Jianwen Bai*

Journal Name: Current Pharmaceutical Biotechnology

Volume 21 , Issue 8 , 2020

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Graphical Abstract:


Objective: To investigate the role of miR-205 and GATA3 in Pulmonary Fibrosis (PF).

Methods: Bleomycin (BLM) was used to induce PF in SD rats and in vitro PF model was established by using TGFβ1-induced RLE-6TN cells. miR-205 mimics were used for the overexpression of miR- 205. The expression of miR-205, GATA3, α-SMA, Collagen I, CHOP and GRP78 were measured using RT-qPCR or western blotting. Dual-luciferase reporter assay was used to confirm binding between GATA3 3’-UTR and miR-205.

Results: The expression of miR-205 was significantly down-regulated, while the expression of GATA3 was remarkably up-regulated in the model rats. GATA3 levels were remarkably decreased when miR-205 was overexpressed. When miR-205 was overexpressed, the lung injury by BLM-induced fibrosis was improved. The expression of α-SMA, Collagen I, as well as GRP78 and CHOP, was significantly up-regulated in both in vivo and in vitro PF models, and overexpression of miR-205 remarkably reversed the effects. Dual-luciferase reporter assay showed that miR-205 directly targeted and negatively regulated GATA3.

Conclusion: miR-205 improved pulmonary fibrosis through inhibiting ER-stress by targeting GATA3.

Keywords: miR-205, pulmonary fibrosis, GATA3, CHOP, endoplasmic reticulum stress, alveolar epithelial cells.

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Article Details

Year: 2020
Page: [720 - 726]
Pages: 7
DOI: 10.2174/1389201021666191210115614
Price: $65

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