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TSP50 通过调节 TGF-β 信号通路介导的肠道黏膜屏障完整性维持来减轻 DSS 诱导的结肠炎。

TSP50 Attenuates DSS-Induced Colitis by Regulating TGF-β Signaling Mediated Maintenance of Intestinal Mucosal Barrier Integrity.

机构信息

NMPA Key Laboratory for Quality Control of Cell and Gene Therapy Medicine Products, Northeast Normal University, Changchun, 130024, China.

National Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun, 130117, China.

出版信息

Adv Sci (Weinh). 2024 Mar;11(11):e2305893. doi: 10.1002/advs.202305893. Epub 2024 Jan 8.

DOI:10.1002/advs.202305893
PMID:38189580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10953580/
Abstract

The integrity of the intestinal mucosal barrier is crucial for protecting the intestinal epithelium against invasion by commensal bacteria and pathogens, thereby combating colitis. The investigation revealed that the absence of TSP50 compromised the integrity of the intestinal mucosal barrier in murine subjects. This disruption facilitated direct contact between intestinal bacteria and the intestinal epithelium, thereby increasing susceptibility to colitis. Mechanistic analysis indicated that TSP50 deficiency in intestinal stem cells (ISCs) triggered aberrant activation of the TGF-β signaling pathway and impeded the differentiation of goblet cells in mice, leading to impairment of mucosal permeability. By inhibiting the TGF-β pathway, the functionality of the intestinal mucosal barrier is successfully restored and mitigated colitis in TSP50-deficient mice. In conclusion, TSP50 played a crucial role in maintaining the intestinal mucosal barrier function and exhibited the preventive effect against the development of colitis by regulating the TGF-β signaling pathway.

摘要

肠道黏膜屏障的完整性对于保护肠道上皮免受共生细菌和病原体的侵袭至关重要，从而对抗结肠炎。研究表明，TSP50 的缺失会损害小鼠肠道黏膜屏障的完整性。这种破坏促进了肠道细菌与肠道上皮的直接接触，从而增加了结肠炎的易感性。机制分析表明，肠道干细胞（ISCs）中 TSP50 的缺失会触发 TGF-β 信号通路的异常激活，并阻碍小鼠杯状细胞的分化，导致黏膜通透性受损。通过抑制 TGF-β 通路，可以成功恢复肠道黏膜屏障的功能，并减轻 TSP50 缺陷小鼠的结肠炎。总之，TSP50 在维持肠道黏膜屏障功能方面发挥着关键作用，并通过调节 TGF-β 信号通路发挥预防结肠炎发展的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/cb3f02b68530/ADVS-11-2305893-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/51693fa115aa/ADVS-11-2305893-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/90d1667adea4/ADVS-11-2305893-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/9e77d4db4bec/ADVS-11-2305893-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/df146af0cac8/ADVS-11-2305893-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/e7bc6ec2f186/ADVS-11-2305893-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/5fdc833cc4a8/ADVS-11-2305893-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/cb3f02b68530/ADVS-11-2305893-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/51693fa115aa/ADVS-11-2305893-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/90d1667adea4/ADVS-11-2305893-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/9e77d4db4bec/ADVS-11-2305893-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/df146af0cac8/ADVS-11-2305893-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/e7bc6ec2f186/ADVS-11-2305893-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/5fdc833cc4a8/ADVS-11-2305893-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/540a/10953580/cb3f02b68530/ADVS-11-2305893-g008.jpg

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