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.
Highlights
Myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSC) plays an important role in idiopathic pulmonary fibrosis
It is generally believed that tissue MSCs exist in almost all tissues including the lungs[6], and an increasing number of studies have shown that lung resident mesenchymal stem cells (LR-MSCs) may be more efficient than bone marrow MSCs (BM-MSCs) from a therapeutic perspective[7]
We investigated the role of miRNA in TGF-β1 -induced myofibroblast differentiation of LR-MSCs and tried to determine whether this could provide a mechanistic explanation for the pathogenesis of lung fibrosis, which may facilitate the development of effective treatment strategies
Summary
Myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSC) plays an important role in idiopathic pulmonary fibrosis. It is generally believed that tissue MSCs exist in almost all tissues including the lungs[6], and an increasing number of studies have shown that lung resident mesenchymal stem cells (LR-MSCs) may be more efficient than BM-MSCs from a therapeutic perspective[7]. These LR-MSCs regulate the repair process by differentiation into several cell types, which may participate in lung repair or contribute to the development of pulmonary diseases. Transforming growth factor β1 (TGF-β1) is highly expressed in pulmonary fibrosis and generally www.nature.com/scientificreports/
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