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

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

典型Notch信号传导参与肠缺血/再灌注损伤后肠上皮细胞凋亡的调节

DOI:
10.3390/ijms15057883
复制
发表时间:
2014-05-06
影响因子:
5.6
通讯作者:
Yang H
Yang H
中科院分区:
生物学2区
文献类型:
--
作者:
Chen G;Zhang Z;Cheng Y;Xiao W;Qiu Y;Yu M;Sun L;Wang W;Du G;Gu Y;Peng K;Xu C;Yang H

文献摘要

参考文献

被引文献

相似文献

Notch信号在维持肠道稳态方面发挥着关键作用。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C57 BL/6小鼠进行假手术或I/R损伤。在再灌注后12 h收集肠组织样品。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明显增加。肠上皮细胞I/R损伤后Jagged 1、DLL 1、Notch 2和Hes 5的mRNA表达及NICD 2和Hes 5的蛋白表达均显著增加。在体外培养的IEC-6细胞模型中,流式细胞仪分析显示,在缺氧/复氧(H/R)条件下,γ-分泌酶抑制剂DAPT抑制Notch信号和siRNA抑制Hes 5表达均显著增加IEC-6细胞的凋亡。结论:Notch 2/Hes 5信号通路在肠I/R损伤中被激活,参与肠上皮细胞凋亡的调控。
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.
DOI: 10.1101/gad.9.21.2609
发表时间: 1995-11-01
影响因子: 10.5
作者:
BAILEY, AM;POSAKONY, JW
通讯作者: POSAKONY, JW
DOI: 10.1038/nature03659
发表时间: 2005-06-16
期刊: NATURE
影响因子: 64.8
作者:
van Es, JH;van Gijn, ME;Clevers, H
通讯作者: Clevers, H
DOI: 10.1053/jpsu.2002.33884
发表时间: 2002-07-01
影响因子: 2.4
作者:
Kuenzler, KA;Pearson, PY;Schwartz, MZ
通讯作者: Schwartz, MZ
DOI: 10.1371/journal.pone.0076274
发表时间: 2013
期刊: PloS one
影响因子: 3.7
作者:
Chen G;Qiu Y;Sun L;Yu M;Wang W;Xiao W;Yang Y;Liu Y;Yang S;Teitelbaum DH;Ma Y;Lu D;Yang H
通讯作者: Yang H
角质形成细胞生长因子改善小鼠肠缺血/再灌注模型的上皮结构和功能
DOI: 10.1371/journal.pone.0044772
发表时间: 2012
期刊: PloS one
影响因子: 3.7
作者:
Cai Y;Wang W;Liang H;Sun L;Teitelbaum DH;Yang H
通讯作者: Yang H