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.
【24h】

S100A4 expression is increased in stricture fibroblasts from patients with fibrostenosing Crohn's disease and promotes intestinal fibroblast migration.

机译:在患有纤维收缩性克罗恩氏病的患者的狭窄成纤维细胞中,S100A4表达增加,并促进肠道成纤维细胞迁移。

获取原文
获取原文并翻译 | 示例
       

摘要

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狭窄克罗恩病(FCD)发病机理中的关键细胞类型。 S100A4是EF手钙结合蛋白家族成员,与上皮-间质转化有关,在慢性组织重塑中作为活化T淋巴细胞和成纤维细胞的标志物。这项研究的目的是检查S100A4在FCD患者切除的回肠中的表达情况。从FCD患者的回盲肠切除术的病变和近端,宏观正常边缘切取粘膜,血清肌外植体和透壁活检。对样品进行了组织化学,免疫组织化学,实时RT-PCR,Western印迹和透射电镜检查。将血清肌成纤维细胞的原代外植培养物暴露于转化生长因子(TGF)-beta1(1 ng / ml),并在24 h评估S100A4的表达和划痕伤口愈合活性。用S100A4小干扰RNA转染CCD-18Co成纤维细胞,用TGF-beta1(1 ng / ml)处理30分钟或24小时,然后评估S100A4和Smad3的表达以及划痕伤口愈合活性。在狭窄的粘膜,固有层和CD3阳性上皮内CD3阳性T淋巴细胞中,S100A4表达增加。在血清肌瘢痕组织中观察到成纤维细胞S100A4染色。严格的成纤维细胞外植体培养显示S100A4表达明显上调。 TGF-beta1增加了培养的回肠成纤维细胞中S100A4的表达。在CCD-18Co成纤维细胞中,S100A4小干扰RNA抑制了刮擦伤口的愈合,并适度抑制了Smad3的激活。 S100A4表达在成纤维细胞以及免疫细胞中在克罗恩病狭窄中增加,并由TGF-beta1诱导。组合实验的结果表明,S100A4在介导肠​​道成纤维细胞迁移中具有潜在作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号