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Butyrate Enhances Intestinal Epithelial Barrier Function via Up-Regulation of Tight Junction Protein Claudin-1 Transcription
Wang, Hong-Bo; Wang, Peng-Yuan; Wang, Xin; Wan, Yuan-Lian; Liu, Yu-Cun
关键词Intestinal epithelium Tight junction Butyrate Claudin-1 Transcription
刊名DIGESTIVE DISEASES AND SCIENCES
2012-12-01
DOI10.1007/s10620-012-2259-4
57期:12页:3126-3135
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Gastroenterology & Hepatology
资助者National natural science foundation of China ; National natural science foundation of China
研究领域[WOS]Gastroenterology & Hepatology
关键词[WOS]HISTONE DEACETYLASE INHIBITORS ; COLON-CANCER ; CELLS ; EXPRESSION ; DIFFERENTIATION ; PROLIFERATION ; MODULATION ; OCCLUDIN ; INJURY ; GENE
英文摘要

Barrier function is essential for the maintenance of normal intestinal function. Dysregulation of the intestinal barrier underlies a wide range of disorders.

Previously, we found that sodium butyrate (NaB) decreased the molecular permeability of intestinal barrier in vivo model, but the mechanism by which NaB facilitated the tightness of tight junctions (TJs) in small intestinal epithelium needed further studies.

In vitro culture of the cdx2-IEC monolayer was used to mimic barrier function. The TJs were assessed by transepithelial electrical resistance (TEER) and paracellular flux of fluorescein isothiocyanate-conjugated dextran 40,000 (FD-40), Western blot, Q-RT-PCR, and immunofluorescence. Promoter and chromatin immunoprecipitation (ChIP) assays were also done to analyze the Claudin-1 gene.

NaB decreased FD-40 flux, increased TEER and TJ protein Claudin-1 expression, induced ZO-1 and Occludin redistribution in cellular membrane, and reversed the damage effect after calcium (Ca2+) switch assay. Silencing Claudin-1 prevented protective function of NaB from enhancing intestinal barrier integrity. Further studies demonstrated that NaB increased Claudin-1 transcription by facilitating the interaction between transcription factor SP1 and a specific motif within the promoter region of Claudin-1. This SP1 binding motif was located upstream of the coding region (-138 to -76 bp) and indispensable for the transcription of Claudin-1 following NaB treatment. ChIP assay confirmed the association between SP1 and Claudin-1 promoter, and the elimination of the SP1 binding site by point mutation resulted in a significant loss of Claudin-1 transcription after NaB dealing.

NaB enhanced intestinal barrier function through increasing Claudin-1 transcription via facilitating the association between SP1 and Claudin-1 promoter.

语种英语
所属项目编号31040041
资助者National natural science foundation of China ; National natural science foundation of China
WOS记录号WOS:000311513900015
引用统计
被引频次:62[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61359
专题北京大学第一临床医学院
作者单位Peking Univ, Hosp 1, Div Gen Surg, Beijing 100034, Peoples R China
推荐引用方式
GB/T 7714
Wang, Hong-Bo,Wang, Peng-Yuan,Wang, Xin,et al. Butyrate Enhances Intestinal Epithelial Barrier Function via Up-Regulation of Tight Junction Protein Claudin-1 Transcription[J]. DIGESTIVE DISEASES AND SCIENCES,2012,57(12):3126-3135.
APA Wang, Hong-Bo,Wang, Peng-Yuan,Wang, Xin,Wan, Yuan-Lian,&Liu, Yu-Cun.(2012).Butyrate Enhances Intestinal Epithelial Barrier Function via Up-Regulation of Tight Junction Protein Claudin-1 Transcription.DIGESTIVE DISEASES AND SCIENCES,57(12),3126-3135.
MLA Wang, Hong-Bo,et al."Butyrate Enhances Intestinal Epithelial Barrier Function via Up-Regulation of Tight Junction Protein Claudin-1 Transcription".DIGESTIVE DISEASES AND SCIENCES 57.12(2012):3126-3135.
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