Abstract
Myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSC) plays an important role in idiopathic pulmonary fibrosis. By comparing the expression profiles of miRNAs before and after myofibroblast differentiation of LR-MSC, we identified miR-877-3p as a fibrosis-related miRNA. We found that miR-877-3p sequestration inhibited the myofibroblast differentiation of LR-MSC and attenuates bleomycin-induced lung fibrosis by targeting Smad7. Smad7, as an inhibitory smad in the TGF-β1 signaling pathway, was decreased in the myofibroblast differentiation of LR-MSC and up-regulation of Smad7 could inhibit the differentiation process. Our data implicates a potential application of miR-877-3p as a fibrosis suppressor for pulmonary fibrosis therapy and also as a fibrosis marker for predicting prognosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bleomycin / pharmacology
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Cell Differentiation / drug effects
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Cell Differentiation / physiology*
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Fibroblasts / drug effects
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Fibroblasts / metabolism
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Fibroblasts / physiology
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Idiopathic Pulmonary Fibrosis / chemically induced
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Idiopathic Pulmonary Fibrosis / metabolism*
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Idiopathic Pulmonary Fibrosis / physiopathology*
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Lung / drug effects
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Lung / metabolism
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Male
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Mesenchymal Stem Cells / metabolism
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Mice
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Mice, Inbred C57BL
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MicroRNAs / metabolism*
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Myofibroblasts / metabolism*
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Myofibroblasts / physiology*
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Signal Transduction / physiology
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Smad7 Protein / metabolism*
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Transforming Growth Factor beta1 / metabolism
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Up-Regulation / physiology
Substances
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MIRN877 microRNA, human
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MicroRNAs
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SMAD7 protein, human
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Smad7 Protein
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Transforming Growth Factor beta1
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Bleomycin