首页> 外文期刊>American Journal of Physiology >S100A4 expression is increased in stricture fibroblasts from patients with fibrostenosing Crohn's disease and promotes intestinal fibroblast migration.
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S100A4 expression is increased in stricture fibroblasts from patients with fibrostenosing Crohn's disease and promotes intestinal fibroblast migration.

机译:S100A4表达在纤维化酵母患者患者的狭窄成纤维细胞中增加,促进肠成纤维细胞迁移。

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Fibroblasts represent the key cell type in fibrostenosing Crohn's disease (FCD) pathogenesis. S100A4 is an EF-hand calcium-binding protein family member, implicated in epithelial-mesenchymal transition and as a marker of activated T lymphocytes and fibroblasts in chronic tissue remodeling. The aim of this study was to examine the expression profile of S100A4 in the resected ileum of patients with FCD. Mucosa, seromuscular explants, and transmural biopsies were harvested from diseased and proximal, macroscopically normal margins of ileocecal resections from patients with FCD. Samples were processed for histochemistry, immunohistochemistry, real-time RT-PCR, Western blotting, and transmission electron microscopy. Primary explant cultures of seromuscular fibroblasts were exposed to transforming growth factor (TGF)-beta1 (1 ng/ml), and S100A4 expression and scratch wound-healing activity were assessed at 24 h. CCD-18Co fibroblasts were transfected with S100A4 small interfering RNA, treated with TGF-beta1 (1 ng/ml) for 30 min or 24 h, and then assessed for S100A4 and Smad3 expression and scratch wound-healing activity. S100A4 expression was increased in stricture mucosa, in the lamina propria, and in CD3-positive intraepithelial CD3-positive T lymphocytes. Fibroblastic S100A4 staining was observed in seromuscular scar tissue. Stricture fibroblast explant culture showed significant upregulation of S100A4 expression. TGF-beta1 increased S100A4 expression in cultured ileal fibroblasts. In CCD-18Co fibroblasts, S100A4 small interfering RNA inhibited scratch wound healing and modestly inhibited Smad3 activation. S100A4 expression is increased in fibroblasts, as well as immune cells, in Crohn's disease stricture and induced by TGF-beta1. Results from knockdown experiments indicate a potential role for S100A4 in mediating intestinal fibroblast migration.
机译:成纤维细胞代表纤维化蛋白酶疾病(FCD)发病机制的关键细胞类型。 S100A4是一种EF-HAND钙结合蛋白家族成员,其具有上皮 - 间充质转换,作为活性T淋巴细胞和成纤维细胞的标志物,慢性组织重塑。本研究的目的是检查FCD患者切除的ELEUM中S100A4的表达谱。从FCD患者的患者中收获粘膜,血清血管外植体和透射活组织检查,从患病患者的患者的患者的患者的患者近似。用于组织化学,免疫组织化学,实时RT-PCR,Western印迹和透射电子显微镜的样品。血清血管成纤维细胞的主要外部外显性培养物暴露于转化生长因子(TGF)-Beta1(1ng / ml),并在24小时评估S100A4表达和划伤伤口愈合活性。用S100A4小干扰RNA转染CCD-18CO成纤维细胞,用TGF-β1(1ng / mL)处理30分钟或24小时,然后评估S100A4和SMAD3表达并划伤伤口愈合活性。 S100A4表达在狭窄的粘膜中升高,在椎板肝癌中,并含有CD3阳性初始性CD3阳性T淋巴细胞。在丝状瘢痕组织中观察到纤维细胞S100A4染色。狭窄的成纤维细胞外植体培养显示S100A4表达的显着上调。 TGF-β1增加培养的髂骨成纤维细胞中的S100A4表达。在CCD-18CO成纤维细胞中,S100A4小干扰RNA抑制划痕伤口愈合,纯度抑制SMAD3活化。 S100A4表达在克罗恩病狭窄中的成纤维细胞以及免疫细胞中增加并受TGF-β1诱导的。敲低实验的结果表明S100A4在介导肠​​成纤维细胞迁移方面的潜在作用。

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