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经典的 Notch 信号通路参与了肠缺血/再灌注损伤后肠道上皮细胞凋亡的调控。

The canonical Notch signaling was involved in the regulation of intestinal epithelial cells apoptosis after intestinal ischemia/reperfusion injury.

机构信息

Department of General Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.

出版信息

Int J Mol Sci. 2014 May 6;15(5):7883-96. doi: 10.3390/ijms15057883.

DOI:10.3390/ijms15057883
PMID:24806344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4057709/
Abstract

Notch signaling plays a critical role in the maintenance of intestinal homeostasis. The aim of the present study was to investigate the role of Notch signaling in the apoptosis of intestinal epithelial cells after intestinal ischemia reperfusion (I/R) injury. Male C57BL/6 mice were subjected to sham operation or I/R injury. Intestinal tissue samples were collected at 12 h after reperfusion. TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling) staining showed that intestinal I/R injury induced significantly increased apoptosis of intestinal epithelial cells. Meanwhile, the mRNA expression of Jagged1, DLL1, Notch2, and Hes5, and protein expression of NICD2 and Hes5 were increased significantly after I/R injury in intestinal epithelial cells. In an in vitro IEC-6 culture model, flow cytometry analyses showed that inhibition of Notch signaling by γ-secretase inhibitor DAPT and the suppression of Hes5 expression using siRNA both significantly increased the apoptosis of IEC-6 cells under the condition of hypoxia/ reoxygenation (H/R). In conclusion, the Notch2/Hes5 signaling pathway was activated and involved in the regulation of intestinal epithelial cells apoptosis in intestinal I/R injury.

摘要

Notch 信号通路在维持肠道内稳态中发挥着关键作用。本研究旨在探讨 Notch 信号通路在肠缺血再灌注（I/R）损伤后肠上皮细胞凋亡中的作用。雄性 C57BL/6 小鼠接受假手术或 I/R 损伤。再灌注后 12 小时采集肠组织样本。TUNEL（末端脱氧核苷酸转移酶介导的 dUTP 生物素缺口末端标记）染色显示，肠 I/R 损伤诱导肠上皮细胞凋亡显著增加。同时，Jagged1、DLL1、Notch2 和 Hes5 的 mRNA 表达以及 NICD2 和 Hes5 的蛋白表达在肠上皮细胞 I/R 损伤后均显著增加。在体外 IEC-6 培养模型中，流式细胞术分析显示，Notch 信号通路的 γ-分泌酶抑制剂 DAPT 抑制和使用 siRNA 抑制 Hes5 表达均显著增加缺氧/复氧（H/R）条件下 IEC-6 细胞的凋亡。综上所述，Notch2/Hes5 信号通路在肠 I/R 损伤中被激活并参与了肠上皮细胞凋亡的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/a407c4539718/ijms-15-07883f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/dfcfa3e146e6/ijms-15-07883f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/82d704db65ba/ijms-15-07883f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/e810b62d22ba/ijms-15-07883f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/695486c344ad/ijms-15-07883f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/a407c4539718/ijms-15-07883f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/dfcfa3e146e6/ijms-15-07883f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/82d704db65ba/ijms-15-07883f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/e810b62d22ba/ijms-15-07883f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/695486c344ad/ijms-15-07883f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a190/4057709/a407c4539718/ijms-15-07883f5.jpg

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