J Biol Regul Homeost Agents. 2019 Sep 26;33(5). doi: 10.23812/19-41A. [Epub ahead of print]
microRNA-155 attenuates profibrotic effects of transforming growth factor-beta on human lung fibroblasts.
- 1 School of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
- 2 Institute of Occupational Medicine, Zhejiang Academy of Medical Sciences, Hangzhou, Zhejiang, China.
- 3 Department of General Surgery, Zhejiang Rehabilitation Medical Center, Hangzhou, Zhejiang, China.
- # Contributed equally
Transforming growth factor-beta (TGF-β) functions in fibrogenesis as a profibrotic mediator, regulating cell proliferation, migration, apoptosis and collagen production of fibroblasts. microRNA-155 (miR-155), the expression of which has been related to bleomycin-induced idiopathic pulmonary fibrosis, has been involved in TGF-β induced epithelial-mesenchymal transition. Here, we found that miR-155 expression was decreased in human pulmonary fibroblasts by TGF-β treatment. We overexpressed miR-155 in fibroblasts to investigate the functional impact of miR-155 on TGF-β-induced fibrotic phenotype of fibroblasts. It is suggested that miR-155 overexpression attenuated the stimulatory effect of TGF-β on fibroblast proliferation, migration and collagen synthesis, by evidence from assessment of cell cycle, viability, apoptosis, migration and collagen content. Furthermore, quantitative measurement showed that SMAD1 gene expression was decreased following miR-155 inhibition, thereby demonstrating an indirect miRNA-SMAD interaction that links miR-155 to TGF-β signaling. Our work helped uncover an miRNA-mediated mechanism of fibroblast response to TGF-β. Moreover, it will help to achieve a better understanding of the regulatory roles of miR-155 in fibrogenesis.
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SMAD proteins, fibroblasts, miRNA, pulmonary fibrosis, transforming growth factor beta
- Journal Article