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Mesenchymal stem cell-derived extracellular vesicles suppress the fibroblast proliferation by downregulating FZD6 expression in fibroblasts via micrRNA-29b-3p in idiopathic pulmonary fibrosis.
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-06-17 , DOI: 10.1002/jcp.29706 Xuan Wan 1 , Shuyun Chen 1 , Yan Fang 2 , Wei Zuo 1 , Jian Cui 1 , Shiguang Xie 1
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-06-17 , DOI: 10.1002/jcp.29706 Xuan Wan 1 , Shuyun Chen 1 , Yan Fang 2 , Wei Zuo 1 , Jian Cui 1 , Shiguang Xie 1
Affiliation
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Idiopathic pulmonary fibrosis (IPF), a progressive and fatal lung disease, usually leads to an irreversible distortion of the pulmonary structure. The functional roles of bone marrow‐derived mesenchymal stem cells (BMSC)‐secreted extracellular vesicles (EVs) in fibroblasts have been implicated, yet their actions in the treatment of IPF are not fully understood. This study investigated the roles of BMSC‐derived EVs expressing miR‐29b‐3p in fibroblasts in IPF treatment. EVs derived from BMSCs were successfully isolated and could be internalized by pulmonary fibroblasts, and Cell Counting Kit‐8 (CCK‐8) and Transwell assay results identified that EVs inhibited the activation of fibroblast in IPF. miR‐29b‐3p, frizzled 6 (FZD6), α‐skeletal muscle actin (α‐SMA), and Collagen I expressions were examined, which revealed that miR‐29b‐3p was poorly expressed and FZD6, α‐SMA, and Collagen I were overexpressed in pulmonary tissues. Dual‐luciferase reporter assay results demonstrated that miR‐29b‐3p could inversely target FZD6 expression. The gain‐ and loss‐of‐function assays were conducted to determine regulatory effects of FZD6 and miR‐29b‐3p on IPF. CCK‐8 and Transwell assays results displayed that BMSCs‐derived EVs overexpressing miR‐29b‐3p contributed to inhibited pulmonary interstitial fibroblast proliferation, migration, invasion, and differentiation. Furthermore, the effects of BMSCs‐derived EVs overexpressing miR‐29b‐3p on IPF progression were assessed in vivo, which confirmed the repressive effects of BMSCs‐derived EVs overexpressing miR‐29b‐3p on IPF progression. Collectively, BMSCs‐derived EVs overexpressing miR‐29b‐3p relieve IPF through FZD6.
中文翻译：
间充质干细胞衍生的细胞外泡通过特发性肺纤维化中通过micrRNA-29b-3p下调成纤维细胞中FZD6的表达来抑制成纤维细胞的增殖。
特发性肺纤维化（IPF）是一种进行性和致命性的肺部疾病，通常会导致不可逆的肺部结构变形。骨髓间充质干细胞（BMSC）分泌的细胞外囊泡（EVs）在成纤维细胞中的功能作用已有牵连，但它们在IPF治疗中的作用尚不完全清楚。这项研究调查了IPF治疗中成纤维细胞中表达miR‐29b‐3p的BMSC衍生电动车的作用。成功地分离了源自BMSC的EV，并且可以被肺成纤维细胞内化，Cell Counting Kit-8（CCK-8）和Transwell分析结果表明，EV抑制了IPF中的成纤维细胞活化。检查了miR‐29b‐3p，卷曲的6（FZD6），α骨骼肌肌动蛋白（α‐SMA）和I型胶原的表达，这表明miR‐29b‐3p在肺组织中表达不佳，FZD6，α‐SMA和胶原I过度表达。双荧光素酶报告基因检测结果表明，miR-29b-3p可以反向靶向FZD6表达。进行功能增强和丧失功能测定以确定FZD6和miR‐29b‐3p对IPF的调节作用。CCK-8和Transwell分析结果表明，过度表达miR-29b-3p的BMSCs衍生的电动汽车可抑制肺间质成纤维细胞的增殖，迁移，侵袭和分化。此外，在体内评估了BMSCs衍生的EVs过表达miR‐29b‐3p对IPF进展的影响，这证实了BMSCs衍生的EVs过表达miR‐29b‐3p对IPF进展的抑制作用。总的来说，
更新日期：2020-06-17
中文翻译：
间充质干细胞衍生的细胞外泡通过特发性肺纤维化中通过micrRNA-29b-3p下调成纤维细胞中FZD6的表达来抑制成纤维细胞的增殖。
特发性肺纤维化（IPF）是一种进行性和致命性的肺部疾病，通常会导致不可逆的肺部结构变形。骨髓间充质干细胞（BMSC）分泌的细胞外囊泡（EVs）在成纤维细胞中的功能作用已有牵连，但它们在IPF治疗中的作用尚不完全清楚。这项研究调查了IPF治疗中成纤维细胞中表达miR‐29b‐3p的BMSC衍生电动车的作用。成功地分离了源自BMSC的EV，并且可以被肺成纤维细胞内化，Cell Counting Kit-8（CCK-8）和Transwell分析结果表明，EV抑制了IPF中的成纤维细胞活化。检查了miR‐29b‐3p，卷曲的6（FZD6），α骨骼肌肌动蛋白（α‐SMA）和I型胶原的表达，这表明miR‐29b‐3p在肺组织中表达不佳，FZD6，α‐SMA和胶原I过度表达。双荧光素酶报告基因检测结果表明，miR-29b-3p可以反向靶向FZD6表达。进行功能增强和丧失功能测定以确定FZD6和miR‐29b‐3p对IPF的调节作用。CCK-8和Transwell分析结果表明，过度表达miR-29b-3p的BMSCs衍生的电动汽车可抑制肺间质成纤维细胞的增殖，迁移，侵袭和分化。此外，在体内评估了BMSCs衍生的EVs过表达miR‐29b‐3p对IPF进展的影响，这证实了BMSCs衍生的EVs过表达miR‐29b‐3p对IPF进展的抑制作用。总的来说，
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