在表达主导负N-cadherin的小鼠中的炎症性肠病和腺瘤
1Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Science (New York, N.Y.)
|November 17, 1995
概括
改变小鼠肠干细胞中的卡德林功能,诱导了炎症性肠病和腺瘤. 这项研究模型是人类克罗恩氏瘤.
科学领域:
- 细胞生物学 细胞生物学
- 发育生物学是发展生物学.
- 胃肠病学 胃肠病学
背景情况:
- 卡德林对于细胞粘附和组织发育至关重要.
- 细胞粘附的失调与各种疾病有关.
研究的目的:
- 为了研究N-cadherin在成年小鼠肠道中的作用.
- 开发一种研究炎症性肠病和肠道瘤的模型.
主要方法:
- 胚胎干细胞感染具有主导阴性N-cadherin突变体 (NCAD三角形) 的转变.
- 通过将修改后的干细胞引入胚胎囊中,生成嵌合体小鼠.
- 在成年仿真小鼠中分析基因表达和组织病理学.
主要成果:
- 在整个密码-维卢斯轴上,NCAD三角形的表达引起了类似克罗恩病的病理学.
- NCAD delta 干扰了密码细胞的增殖,迁移和亡.
- 在小的局部NCAD三角形表达没有诱导疾病.
结论:
- N-cadherin在维持肠道平衡中起着至关重要的作用.
- 肠干细胞中卡德林功能的干扰可能导致炎症性肠病和腺瘤形成.
- 这种小鼠模型提供了对卡德林功能和肠道疾病病原体的见解.
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