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转录因子 FoxM1 通过激活 Nurr1 促进缺血/再灌注损伤后的肠道再生。

The transcription factor FoxM1 activates Nurr1 to promote intestinal regeneration after ischemia/reperfusion injury.

机构信息

Department of Gastroenterology Surgery, The Dalian Municipal Central Hospital Affiliated of Dalian Medical University, 116033, Dalian, China.

Institute of Integrative Medicine, Dalian Medical University, 116044, Dalian, China.

出版信息

Exp Mol Med. 2019 Nov 8;51(11):1-12. doi: 10.1038/s12276-019-0343-y.

DOI:10.1038/s12276-019-0343-y
PMID:31704909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6841953/
Abstract

FoxM1 is involved in the regeneration of several organs after injury and expressed in the intestinal mucosa. The intrinsic mechanism of FoxM1 activity in the mucosa after intestinal ischemia/reperfusion (I/R) injury has not been reported. Therefore, we investigated the role of FoxM1 in mediating intestinal mucosa regeneration after I/R injury. Expression of FoxM1 and the proliferation of intestinal mucosa epithelial cells were examined in rats with intestinal I/R injury and an IEC-6 cell hypoxia/reperfusion (H/R) model. The effects of FoxM1 inhibition or activation on intestinal epithelial cell proliferation were measured. FoxM1 expression was consistent with the proliferation of intestinal epithelial cells in the intestinal mucosa after I/R injury. Inhibition of FoxM1 expression led to the downregulation of Ki-67 expression mediated by the inhibited expression of Nurr1, and FoxM1 overexpression promoted IEC-6 cell proliferation after H/R injury through activating Nurr1 expression. Furthermore, FoxM1 directly promoted the transcription of Nurr1 by directly binding the promoter of Nurr1. Further investigation showed low expression levels of FoxM1, Nurr1, and Ki-67 in the intestinal epithelium of patients with intestinal ischemic injury. FoxM1 acts as a critical regulator of intestinal regeneration after I/R injury by directly promoting the transcription of Nurr1. The FoxM1/Nurr1 signaling pathway represents a promising therapeutic target for intestinal I/R injury and related clinical diseases.

摘要

FoxM1 参与多种器官损伤后的再生，在肠黏膜中表达。FoxM1 在肠缺血/再灌注 (I/R) 损伤后黏膜中的内在活性机制尚未报道。因此，我们研究了 FoxM1 在介导 I/R 损伤后肠黏膜再生中的作用。在肠 I/R 损伤大鼠和 IEC-6 细胞缺氧/复氧 (H/R) 模型中检测 FoxM1 表达和肠黏膜上皮细胞增殖。测定 FoxM1 抑制或激活对肠上皮细胞增殖的影响。FoxM1 表达与 I/R 损伤后肠黏膜上皮细胞的增殖一致。FoxM1 表达抑制导致 Nurr1 表达抑制介导的 Ki-67 表达下调，FoxM1 过表达通过激活 Nurr1 表达促进 H/R 损伤后 IEC-6 细胞增殖。此外，FoxM1 通过直接结合 Nurr1 启动子直接促进 Nurr1 的转录。进一步研究显示，肠缺血损伤患者肠上皮细胞中 FoxM1、Nurr1 和 Ki-67 表达水平较低。FoxM1 通过直接促进 Nurr1 的转录，作为 I/R 损伤后肠再生的关键调节因子。FoxM1/Nurr1 信号通路为肠 I/R 损伤及相关临床疾病的治疗提供了有前途的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/1343911761b7/12276_2019_343_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/50adb4c029a1/12276_2019_343_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/02dbd3ba432f/12276_2019_343_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/f295c33ce038/12276_2019_343_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/2888a6f2cbfd/12276_2019_343_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/32d7ce429146/12276_2019_343_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/0f8c438fb3a6/12276_2019_343_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/056e630ba0b6/12276_2019_343_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/1343911761b7/12276_2019_343_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/50adb4c029a1/12276_2019_343_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/02dbd3ba432f/12276_2019_343_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/f295c33ce038/12276_2019_343_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/2888a6f2cbfd/12276_2019_343_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/32d7ce429146/12276_2019_343_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/0f8c438fb3a6/12276_2019_343_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/056e630ba0b6/12276_2019_343_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f1c/6841953/1343911761b7/12276_2019_343_Fig8_HTML.jpg

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