Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM). ECM is mainly secreted by myofibroblast which is the activation state of fibroblasts. MicroRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified. In this study, we hypothesized that miR-29b might play a protective role in the progress of silicosis. MTT assay, qRT-PCR, Immunofluorescence and Western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but also was involved in the down-regulation of miR-29b. Meanwhile it could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited the synthesis. These findings indicated that miR-29b inhibited the supernatants from silica-treated macrophages induced extracellular matrix synthesis, and it might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.

中文翻译：

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MicroRNA-29b抑制了来自二氧化硅处理的巨噬细胞诱导的肺成纤维细胞中细胞外基质合成的上清液。

硅肺病的病理特征是弥漫性肺纤维化和细胞外基质（ECM）的大量沉积。ECM主要由成纤维细胞分泌，这是成纤维细胞的活化状态。MicroRNA-29b（miR-29b）是参与纤维化的著名microRNA之一，但尚未明确其在矽肺中的作用。在这项研究中，我们假设miR-29b可能在矽肺病的进展中起保护作用。应用MTT测定，qRT-PCR，免疫荧光和蛋白质印迹。结果表明，二氧化硅处理的巨噬细胞的上清液不仅引起成纤维细胞（NIH-3T3和MRC-5）的增殖，而且还参与了miR-29b的下调。同时，它可以诱导成纤维细胞活化，增加ECM成分（如胶原蛋白1和胶原蛋白3）的表达，以二氧化硅剂量依赖性方式。此外，通过转染模拟物来过度表达miR-29b会显着降低ECM成分的表达并抑制合成。这些发现表明，miR-29b抑制了二氧化硅处理的巨噬细胞诱导的细胞外基质合成的上清液，并且在矽肺病中可能具有很强的抗纤维化能力，并且可以作为潜在的治疗剂。