STIM1 Deficiency In Intestinal Epithelium Attenuates Colonic Inflammation and Tumorigenesis by Reducing ER Stress of Goblet Cells.

Animals Carcinogenesis / metabolism Cell Transformation, Neoplastic Colitis / chemically induced Colitis-Associated Neoplasms Dextran Sulfate / toxicity Goblet Cells / metabolism Humans Inflammation / metabolism Inflammatory Bowel Diseases Intestinal Mucosa / metabolism Mice Neoplasm Proteins / deficiency Stromal Interaction Molecule 1 / genetics
ER Stress Goblet Cells IBD Mucosal Barrier

Journal

Cellular and molecular gastroenterology and hepatology
ISSN: 2352-345X
Titre abrégé: Cell Mol Gastroenterol Hepatol
Pays: United States
ID NLM: 101648302

Informations de publication

Date de publication:
2022
Historique:
received: 29 09 2021
revised: 23 03 2022
accepted: 24 03 2022
pubmed: 4 4 2022
medline: 22 6 2022
entrez: 3 4 2022
Statut: ppublish

Résumé

As an indispensable component of store-operated Ca Inflammatory and matched normal intestinal tissues were collected from IBD patients to investigate the expression of STIM1. Intestinal epithelium-specific STIM1 conditional knockout mice (STIM1 STIM1 could regulate intestinal epithelial homeostasis. STIM1 was augmented in the inflammatory intestinal tissues of IBD patients. In dextran sodium sulfate-induced colitis, STIM1 deficiency in intestinal epithelium reduced the loss of goblet cells through alleviating endoplasmic reticulum stress induced by disturbed Ca Our results establish STIM1 as a crucial regulator for the maintenance of the intestinal barrier during colitis and provide a potential target for IBD treatment.

Sections du résumé

BACKGROUND & AIMS
As an indispensable component of store-operated Ca
METHODS
Inflammatory and matched normal intestinal tissues were collected from IBD patients to investigate the expression of STIM1. Intestinal epithelium-specific STIM1 conditional knockout mice (STIM1
RESULTS
STIM1 could regulate intestinal epithelial homeostasis. STIM1 was augmented in the inflammatory intestinal tissues of IBD patients. In dextran sodium sulfate-induced colitis, STIM1 deficiency in intestinal epithelium reduced the loss of goblet cells through alleviating endoplasmic reticulum stress induced by disturbed Ca
CONCLUSIONS
Our results establish STIM1 as a crucial regulator for the maintenance of the intestinal barrier during colitis and provide a potential target for IBD treatment.

Identifiants

DOI: 10.1016/j.jcmgh.2022.03.007 PMID: 35367664 PMC: PMC9130113
pubmed: 35367664
pii: S2352-345X(22)00059-5
doi: 10.1016/j.jcmgh.2022.03.007
pmc: PMC9130113
pii:
doi:

Substances chimiques

Neoplasm Proteins 0
STIM1 protein, human 0
Stim1 protein, mouse 0
Stromal Interaction Molecule 1 0
Dextran Sulfate 9042-14-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

193-217

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Xiaojing Liang (X)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Jiansheng Xie (J)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Hao Liu (H)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Rongjie Zhao (R)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Wei Zhang (W)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Haidong Wang (H)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Hongming Pan (H)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China.

Yubin Zhou (Y)

Center for Translational Cancer Research, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas.

Weidong Han (W)

Department of Medical Oncology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China. Electronic address: hanwd@zju.edu.cn.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Processus néoplasiques › Carcinogenèse › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Processus néoplasiques › Carcinogenèse › Transformation cellulaire néoplasique › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › Maladies de l'appareil digestif › Maladies gastro-intestinales › Maladies intestinales › Maladies du côlon › Colite › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › Maladies de l'appareil digestif › Maladies gastro-intestinales › Maladies intestinales › Tumeurs de l'intestin › Tumeurs du côlon › Néoplasmes associés aux colites › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › Glucides › Polyosides › Glucanes › Dextrane › Sulfate dextran › STIM1 Deficiency In Intestinal Epithelium...
questionsmedicales.fr › Cellules › Cellules épithéliales › Cellules caliciformes › STIM1 Deficiency In Intestinal Epithelium...
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questionsmedicales.fr › Maladies de l'appareil digestif › Maladies gastro-intestinales › Maladies intestinales › Maladies inflammatoires intestinales › STIM1 Deficiency In Intestinal Epithelium...
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