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首页> 外文期刊>Cell and Tissue Research >Interference of miR-943-3p with secreted frizzled-related proteins4 (SFRP4) in an asthma mouse model
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Interference of miR-943-3p with secreted frizzled-related proteins4 (SFRP4) in an asthma mouse model

机译：MiR-943-3P在哮喘小鼠模型中与分泌细胞混发相关的蛋白质4（SFRP4）的干扰

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摘要

The aim of this study is to investigate the potential roles of miR-943-3p and its target gene secreted frizzled-related proteins4 (SFRP4) in allergic asthma and elucidate its underlying mechanism, which may prompt a new clue about developing novel treatments of this disease. An allergic asthma mouse model was generated by challenging with ovalbumin (OVA); lung pathological features of mice were viewed using H&E staining; thickness of subepithelial fibrosis and smooth muscle was measured using Masson's trichrome staining. Inflammatory cells from bronchoalveolar lavage fluid (BALF) were counted based on Diff-Quik staining and morphometric analysis. Expressions of miR-943-3p, SFRP4 and Wnt signal pathway-associated proteins were detected using RT-PCR or immunoblotting, respectively. SFRP4 was downregulated in the bronchial biopsies of allergic asthma patients and represented a unique intersection between differentially expressed genes (DEGs) and genes in the Wnt signal pathway. Both miR-943-3p upregulation and SFRP4 downregulation were detected in allergic asthma patients and OVA-induced mice. Besides, OVA-induced mice possessed more inflammatory cells in BALF including macrophage (mac), eosinophil (eos), lymphocyte (lym) and neutrophil (neu), higher expression of collagen, beta-catenin and c-Myc as well as thicker subepithelial fibrosis and smooth muscle in lung than control mice. In vivo delivery of miR-943-3p agomir worsened these symptoms, while both miR-943-3p antagomir and Ad-SFRP4 administration effectively alleviated this disease. Taken together, miR-943-3p accelerated the progression of airway inflammation and remodeling in allergic asthma via suppressing the activity of SFRP4 through Wnt signaling pathway in asthma patients and OVA-induced mice.
机译：本研究的目的是探讨miR-943-3p及其靶基因分泌的毛毡相关蛋白质4（sfrp4）的潜在作用，并阐明其潜在机制，这可能会提示新的CO.CUE开发新的治疗方法疾病。通过用卵巢（OVA）挑战，产生过敏性哮喘小鼠模型;使用H＆E染色观察小鼠的肺病理特征;使用Masson的三色染色来测量耻骨上纤维化和平滑肌的厚度。基于Diff-Quik染色和形态学分析计数来自支气管肺泡灌洗液（BALF）的炎症细胞。使用RT-PCR或免疫印迹检测miR-943-3p，sfrp4和wnt信号途径相关蛋白的表达。 SFRP4在过敏性哮喘患者的支气管活组织检查中下调，代表了WNT信号途径中的差异表达基因（DEGS）和基因之间的独特交叉。在过敏性哮喘患者和OVA诱导的小鼠中检测到MIR-943-3P上调和SFRP4下调。此外，OVA诱导的小鼠在BALF中具有更多的炎症细胞，包括巨噬细胞（MAC），嗜酸性粒细胞（EOS），淋巴细胞（LYM）和中性粒细胞（NEU），胶原蛋白，β-连环蛋白和C-MYC的更高表达以及较厚的亚脑皮蠕虫和肺部平滑肌比对照小鼠。体内交付miR-943-3p Agomir恶化了这些症状，而MiR-943-3P antagomir和Ad-SFRP4管理局则有效地缓解了这种疾病。 MiR-943-3P通过抑制哮喘患者和OVA诱导的小鼠的WNT信号通路，加速了气道炎症和过敏性哮喘重塑的进展。

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