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miR-200b 参与克罗恩病的肠道纤维化。

miR-200b is involved in intestinal fibrosis of Crohn's disease.

机构信息

Department of Gastroenterology, Shanghai Jiao Tong University, School of Medicine, Xin Hua Hospital, Shanghai, PR China.

出版信息

Int J Mol Med. 2012 Apr;29(4):601-6. doi: 10.3892/ijmm.2012.894. Epub 2012 Jan 23.

DOI:10.3892/ijmm.2012.894
PMID:22294131
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3573760/
Abstract

Intestinal fibrosis is one of the major serious complications of Crohn's disease (CD). However, there are no effective antifibrotic drugs to treat intestinal fibrosis in CD. Therefore, it is important to understand the pathogenesis of fibrosis in CD. It has been reported that members of the miR-200 family are essential in the regulation of renal fibrogenesis. In this study, we analyzed the function of miR-200a and miR-200b in intestinal fibrosis, which was induced by transforming growth factor β1 (TGF-β1) in vitro. Furthermore, we detected the expression of miR-200a and miR-200b in CD specimens, which were divided into groups of fibrosis and no-fibrosis. The results of this study showed that administration of miR-200b could partially protect intestinal epithelial cells from fibrogenesis in vitro. Furthermore, we found that miR-200b was overexpressed in the serum of the fibrosis group. The results suggest that miR-200b has potential value for diagnostic and therapeutic applications for CD patients with fibrosis complications.

摘要

肠纤维化是克罗恩病（CD）的主要严重并发症之一。然而，目前尚无有效的抗纤维化药物来治疗 CD 中的肠纤维化。因此，了解 CD 中纤维化的发病机制很重要。据报道，miR-200 家族成员在调节肾纤维化中起着重要作用。在这项研究中，我们分析了 miR-200a 和 miR-200b 在体外转化生长因子 β1（TGF-β1）诱导的肠纤维化中的作用。此外，我们检测了 CD 标本中 miR-200a 和 miR-200b 的表达，这些标本分为纤维化组和无纤维化组。本研究结果表明，miR-200b 的给药可部分保护体外肠上皮细胞免受纤维化。此外，我们发现纤维化组血清中 miR-200b 表达上调。这些结果表明，miR-200b 对诊断和治疗 CD 伴有纤维化并发症的患者具有潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/087e7af7d8fa/IJMM-29-04-0601-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/9aeedde14049/IJMM-29-04-0601-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/893d7c399dd8/IJMM-29-04-0601-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/36edc47c2ca4/IJMM-29-04-0601-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/8a15dbbc48ed/IJMM-29-04-0601-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/087e7af7d8fa/IJMM-29-04-0601-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/9aeedde14049/IJMM-29-04-0601-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/893d7c399dd8/IJMM-29-04-0601-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/36edc47c2ca4/IJMM-29-04-0601-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/8a15dbbc48ed/IJMM-29-04-0601-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/3573760/087e7af7d8fa/IJMM-29-04-0601-g04.jpg

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