相关实验视频

Updated: Jul 19, 2025

Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice

Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice

Published on: July 12, 2018

在小鼠肠道Cdc42的单基性缺陷导致粘膜炎症,诱导密室失生症

Dongsheng Zhang^1,2,3, Wenjuan Tang^3,4, Haitao Niu^5,6

¹Division of Hematology and Oncology, Division of Cancer Biology, Department of Medicine, MetroHealth Medical Center (MHMC), Case Western Reserve University (CWRU), School of Medicine, Cleveland, OH 44109, USA.

Genes & diseases

|August 17, 2023

概括

CDC42的枯竭会损害肠道干细胞的再生和修复,导致炎症和潜在的瘤. 结肠中CDC42的损失会减少干细胞,导致炎症和发育不良.

科学领域:

胃肠病学胃肠病学
细胞生物学细胞生物学
在瘤学瘤学.

背景情况:

CDC42调节肠上皮干细胞 (IESC) 的分裂.
异常的CDC42在启动肠道炎症和瘤的作用尚未完全理解.

研究的目的:

研究肠道Cdc42在炎症性肠病 (IBD),结直肠癌,衰老和IESC损伤中的作用.
确定Cdc42损失对IESC再生和肠上皮质修复的影响.

主要方法:

使用IBD,结直肠癌,衰老和IESC损伤的小鼠模型.
使用各种Cre-lox系统 (Villin-Cre,Villin-CreER^T2,Lgr5-eGFP-IRES-CreER^T2,Bmi1-CreER^T2) 产生了Cdc42缺乏的小鼠.
在人类IBD和结直肠癌样本中评估了CDC42水平;在炎症,衰老和损伤的情况下,评估了IESC再生和修复以应对Cdc42耗尽.

主要成果:

结肠直肠癌中增加的CDC42与生存率下降相关,而在炎症IBD结肠中观察到较低的CDC42水平.
结肠Cdc42的耗尽减少了Lgr5+IESCs,增加了前体增生症,诱导了粘膜炎症,并导致了密室失生症.
Cdc42的耗尽加剧了辐射和化学诱导的结肠炎和损伤的结肠Lgr5+ IESC再生.

结论:

减少Cdc42会损害IESC再生和肠上皮的修复,导致长期的粘膜炎症.
构成Cdc42的单一性损失会诱导粘膜炎症,在衰老情况下可能导致肠道瘤.

关键词:

细胞分裂周期42 (CDC42) 的一个例子.大肠炎是什么意思大肠直肠癌 (CRC) 是一种癌症.炎症性肠病 (IBD) 是一种炎症性肠病.肠上皮细胞 (IEC) 是一种肠上皮细胞.肠上皮干细胞 (IESC) 是一种干细胞.辐射辐射是一种辐射.

更多相关视频

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy

Published on: October 6, 2014

Generation of Murine Primary Colon Epithelial Monolayers from Intestinal Crypts

Generation of Murine Primary Colon Epithelial Monolayers from Intestinal Crypts

Published on: February 6, 2021

相关概念视频

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

Renewal of Intestinal Stem Cells

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...