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沙门氏菌通过 Wnt/β-连环蛋白通路调节肠道干细胞。

Salmonella regulation of intestinal stem cells through the Wnt/beta-catenin pathway.

机构信息

Department of Medicine, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.

出版信息

FEBS Lett. 2010 Mar 5;584(5):911-6. doi: 10.1016/j.febslet.2010.01.024. Epub 2010 Jan 19.

DOI:10.1016/j.febslet.2010.01.024
PMID:20083111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2829849/
Abstract

Recent studies have revealed that bacteria target stem cells for long-term survival in a Drosophila model. However, in mammalian models, little is known about bacterial infection and intestinal stem cells. Our study aims at understanding bacterial regulation of the intestinal stem cell in a Salmonella colitis mouse model. We found that Salmonella activates the Wnt/beta-catenin signaling pathway that is known to regulate stem cells. We identified Salmonella protein AvrA that modulates Wnt signaling including upregulating Wnt expression, modifying beta-catenin, increasing total beta-catenin expression, and activating Wnt/beta-catenin transcriptional activity in the intestinal epithelial cells. The numbers of stem cells and proliferative cells increased in the intestine infected with Salmonella expressing AvrA. Our study provides insights into bacterial infection and stem cell maintenance.

摘要

最近的研究表明,细菌在果蝇模型中为了长期生存而将目标对准干细胞。然而,在哺乳动物模型中,人们对细菌感染和肠道干细胞知之甚少。我们的研究旨在了解沙门氏菌结肠炎小鼠模型中细菌对肠道干细胞的调节。我们发现沙门氏菌激活了已知调节干细胞的 Wnt/β-连环蛋白信号通路。我们鉴定出沙门氏菌蛋白 AvrA 可调节 Wnt 信号,包括上调 Wnt 表达、修饰β-连环蛋白、增加总β-连环蛋白表达以及激活肠道上皮细胞中的 Wnt/β-连环蛋白转录活性。表达 AvrA 的沙门氏菌感染的肠道中干细胞和增殖细胞的数量增加。我们的研究为细菌感染和干细胞维持提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/b67a615e7285/nihms171247f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/dc0be34ab535/nihms171247f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/13927134eed9/nihms171247f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/f93de41102fb/nihms171247f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/a717418e0f3c/nihms171247f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/b67a615e7285/nihms171247f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/dc0be34ab535/nihms171247f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/13927134eed9/nihms171247f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/f93de41102fb/nihms171247f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/a717418e0f3c/nihms171247f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41b/2829849/b67a615e7285/nihms171247f5.jpg

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Suppression of induced pluripotent stem cell generation by the p53-p21 pathway.p53-p21 通路对诱导多能干细胞生成的抑制作用。
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Genome-wide RNAi screen identifies genes involved in intestinal pathogenic bacterial infection.全基因组RNA干扰筛选鉴定出参与肠道致病性细菌感染的基因。
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Single Lgr5 stem cells build crypt-villus structures in vitro without a mesenchymal niche.单个Lgr5干细胞在体外无需间充质微环境即可构建隐窝-绒毛结构。
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