The anti-fibrotic effects of microRNA-153 by targeting TGFBR-2 in pulmonary fibrosis
| Autor: | Xiaojuan Quan, Lin Zhang, Da-Jiang Cui, Chun-lian Liang, Xiu-li Li, Weilin Yang |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Pulmonary Fibrosis
Blotting Western Clinical Biochemistry Protein Serine-Threonine Kinases Biology Real-Time Polymerase Chain Reaction Bleomycin Pathology and Forensic Medicine Transforming Growth Factor beta1 Mice chemistry.chemical_compound Idiopathic pulmonary fibrosis Cell Movement Cell surface receptor Pulmonary fibrosis medicine Animals Humans RNA Messenger Receptor Lung Molecular Biology Cells Cultured Wound Healing Antibiotics Antineoplastic Reverse Transcriptase Polymerase Chain Reaction Receptor Transforming Growth Factor-beta Type II Fibroblasts medicine.disease Mice Inbred C57BL MicroRNAs medicine.anatomical_structure chemistry Immunology Cancer research Signal transduction Receptors Transforming Growth Factor beta Transforming growth factor |
| Zdroj: | Experimental and Molecular Pathology. 99:279-285 |
| ISSN: | 0014-4800 |
| DOI: | 10.1016/j.yexmp.2015.07.011 |
| Popis: | Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial fibrotic lung disease with an undefined etiology and no effective treatments. By binding to cell surface receptors, transforming growth factor-β (TGF-β) plays a pivotal role in lung fibrosis. Therefore, the screening of microRNAs (miRNAs), especially those interrupting the effects of TGF-β, may provide information not only on the pathomechanism, but also on the treatment of this disease. In the present study, we found that miR-153 expression was dysregulated in the lungs of mice with experimental pulmonary fibrosis and TGF-β1 decreased miR-153 expression in pulmonary fibroblasts. Moreover, increased miR-153 levels attenuated, whereas the knock down of miR-153 promoted the pro-fibrogenic activity of TGF-β1, and miR-153 reduced the contractile and migratory activities of fibroblasts. In addition, TGFBR2, a transmembrane serine/threonine kinase receptor for TGF-β, was identified as a direct target of miR-153. Furthermore, by post-transcriptional regulation of the expression of TGFBR2, phosphorylation of SMAD2/3 was also influenced by miR-153. These data suggest that miR-153 disturbs TGF-β1 signal transduction and its effects on fibroblast activation, acting as an anti-fibrotic element in the development of pulmonary fibrosis. |
| Databáze: | OpenAIRE |
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