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家族基因在人类炎症性肠病中的表达及其调控

Expression of family genes in human inflammatory bowel diseases and its regulation.

作者信息

Tsuchida Chikatsugu, Sakuramoto-Tsuchida Sumiyo, Taked Maiko, Itaya-Hironaka Asako, Yamauchi Akiyo, Misu Masayasu, Shobatake Ryogo, Uchiyama Tomoko, Makino Mai, Pujol-Autonell Irma, Vives-Pi Marta, Ohbayashi Chiho, Takasawa Shin

机构信息

Department of Biochemistry, Nara Medical University, Kashihara 634-8521, Japan.

Saiseikai Nara Hospital, Nara 630-8145, Japan.

出版信息

Biochem Biophys Rep. 2017 Oct 23;12:198-205. doi: 10.1016/j.bbrep.2017.10.003. eCollection 2017 Dec.

DOI:10.1016/j.bbrep.2017.10.003
PMID:29090282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5655384/
Abstract

The pathophysiology of inflammatory bowel disease (IBD) reflects a balance between mucosal injury and reparative mechanisms. Some regenerating gene () family members have been reported to be expressed in Crohn's disease (CD) and ulcerative colitis (UC) and to be involved as proliferative mucosal factors in IBD. However, expression of all family genes in IBD is still unclear. Here, we analyzed expression of all family genes (, , , , and ) in biopsy specimens of UC and CD by real-time RT-PCR. , , and genes were overexpressed in CD samples. gene was also overexpressed in UC samples. We further analyzed the expression mechanisms of , , and genes in human colon cells. The expression of was significantly induced by IL-6 or IL-22, and was induced by IL-22. Deletion analyses revealed that three regions (- 220 to - 211, - 179 to - 156, and - 146 to - 130) in and the region (- 274 to- 260) in promoter were responsible for the activation by IL-22/IL-6. The promoters contain consensus transcription factor binding sequences for MZF1, RTEF1/TEAD4, and STAT3 in , and HLTF/FOXN2F in , respectively. The introduction of siRNAs for MZF1, RTEF1/TEAD4, STAT3, and HLTF/FOXN2F abolished the transcription of and . The gene activation mechanisms of may play a role in colon mucosal regeneration in IBD.

摘要

炎症性肠病（IBD）的病理生理学反映了黏膜损伤与修复机制之间的平衡。据报道，一些再生基因（）家族成员在克罗恩病（CD）和溃疡性结肠炎（UC）中表达，并作为IBD中增殖性黏膜因子发挥作用。然而，IBD中所有家族基因的表达仍不清楚。在此，我们通过实时逆转录聚合酶链反应（RT-PCR）分析了UC和CD活检标本中所有家族基因（、、、、和）的表达。、和基因在CD样本中过表达。基因在UC样本中也过表达。我们进一步分析了、和基因在人结肠细胞中的表达机制。的表达受到白细胞介素-6（IL-6）或白细胞介素-22（IL-22）的显著诱导，而受到IL-22的诱导。缺失分析显示，启动子中的三个区域（-220至-211、-179至-156和-146至-130）以及启动子中的区域（-274至-260）负责IL-22/IL-6的激活。这些启动子分别包含MZF1、RTEF1/TEAD4和STAT3在中的共有转录因子结合序列，以及HLTF/FOXN2F在中的共有转录因子结合序列。针对MZF1、RTEF1/TEAD4、STAT3和HLTF/FOXN2F的小干扰RNA（siRNA）的导入消除了和的转录。的基因激活机制可能在IBD的结肠黏膜再生中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/9e8d0071eca0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/d8b7e1ecee6b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/a3c16c2e6561/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/9ea6647e1682/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/877cb2781d10/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/9e8d0071eca0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/d8b7e1ecee6b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/a3c16c2e6561/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/9ea6647e1682/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/877cb2781d10/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b98/5655384/9e8d0071eca0/gr4.jpg

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