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首页> 外文期刊>International archives of allergy and immunology >MiR-204-5p Inhibits Transforming Growth Factor-beta 1-Induced Proliferation and Extracellular Matrix Production of Airway Smooth Muscle Cells by Regulating Six1 in Asthma
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MiR-204-5p Inhibits Transforming Growth Factor-beta 1-Induced Proliferation and Extracellular Matrix Production of Airway Smooth Muscle Cells by Regulating Six1 in Asthma

机译：MiR-204-5P通过调节哮喘中的61次抑制转化生长因子-β1-诱导的气道平滑肌细胞的细胞外基质生产

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Background: Transforming growth factor-beta 1 (TGF-beta 1)-in-duced proliferation of airway smooth muscle cells plays critical roles in the development of airway remodeling. Six1 (sine oculis homeobox homolog 1) has been demonstrated to be involved in airway inflammation and remodeling in asthmatic mice. Objectives: The aim of this work was to investigate the potential role of miR-204-5p in the proliferation and extracellular matrix (ECM) production of airway smooth muscle cells in asthma. Methods: Real-time PCR was used to measure the expression of miR-204-5p in asthmatic airway smooth muscle cells. Cell viability and apoptosis were detected to evaluate the effect of miR-204-5p on airway smooth muscle cells. Dual-luciferase reporter experiments were applied to identify the target genes of miR-204-5p. Results: MiR-204-5p was downregulated notably in asthmatic airway smooth muscle cells as well as cells stimulated with TGF-beta 1. Overexpression of miR-204-5p markedly suppressed the TGF-beta 1-induced proliferation of airway smooth muscle cells and the deposition of ECM, whereas the inhibition of miR-204-5p significantly enhanced the proliferation of airway smooth muscle cells and upregulated the level of fibronectin and collagen III. Furthermore, subsequent analyses demonstrated that Six1 was a direct target of miR-204-5p, and Western blot further indicated that miR-204-5p negatively regulated the expression of Six1. Most importantly, the restoration of Six1 expression reversed the inhibitory effect of miR-204-5p on TGF-beta 1-induced proliferation and ECM production. Conclusions: MiR-204-5p inhibits TGF-beta 1-in-duced proliferation and ECM production of airway smooth muscle cells by regulating Six1, identifying a potential therapeutic target for preventing airway remodeling in asthma.
机译：背景：转化生长因子-β1（TGF-β1）-IN-CURIAD的气道平滑肌细胞的增殖在气道重塑的发展中起着关键作用。 S161（正弦Oculis Homeobox Homolog 1）已被证明参与哮喘小鼠的气道炎症和重塑。目的：这项工作的目的是探讨miR-204-5p在哮喘中气道平滑肌细胞的增殖和细胞外基质（ECM）生产中miR-204-5p的潜在作用。方法：使用实时PCR测量哮喘呼吸道平滑肌细胞miR-204-5p的表达。检测到细胞活力和细胞凋亡，以评估miR-204-5p对气道平滑肌细胞的影响。施用双荧光素酶报告结果以鉴定miR-204-5p的靶基因。结果：MIR-204-5P显着下调，在哮喘呼吸道平滑肌细胞以及用TGF-β刺激的细胞1. MIR-204-5P的过表达明显抑制了TGF-β1诱导的气道平滑肌细胞增殖ECM的沉积，而MiR-204-5P的抑制显着增强了气道平滑肌细胞的增殖，并上调了纤连蛋白和胶原III的水平。此外，随后的分析证明，S161是miR-204-5p的直接靶标，并且Western印迹进一步表明miR-204-5p对S161的表达负调节。最重要的是，恢复六1表达逆转MIR-204-5P对TGF-β1诱导的增殖和ECM生产的抑制作用。结论：MiR-204-5P通过调节S161来抑制TGF-β1-型增殖和ECM生产气道平滑肌细胞，鉴定用于防止哮喘中的气道重塑的潜在治疗靶标。

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