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Modulation of stem cell fate in intestinal homeostasis,injury and repair

World Journal of Stem Cells 2023年第5期15卷 354-368页

作者： Zhe Wang Yan-Ji Qu Min Cui Department of Gastroenterology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022Hubei ProvinceChina Department of Otorhinolaryngology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022Hubei ProvinceChina Department of Orthopedics Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022Hubei ProvinceChina

The mammalian intestinal epithelium constitutes the largest barrier against the external environment and makes flexible responses to various types of stimuli.epithelial cells are fast-renewed to counteract constant damage and disrupted barrier function to maintain their integrity.The homeostatic repair and regeneration of the intestinal epithelium are governed by the Lgr5+intestinal stem cells(ISCs)located at the base of crypts,which fuel rapid renewal and give rise to the different epithelial cell types.Protracted biological and physicochemical stress may challenge epithelial integrity and the function of ISCs.The field of ISCs is thus of interest for complete mucosal healing,given its relevance to diseases of intestinal injury and inflammation such as inflammatory bowel diseases.Here,we review the current understanding of the signals and mechanisms that control homeostasis and regeneration of the intestinal epithelium.We focus on recent insights into the intrinsic and extrinsic elements involved in the process of intestinal homeostasis,injury,and repair,which fine-tune the balance between self-renewal and cell fate specification in ISCs.Deciphering the regulatory machinery that modulates stem cell fate would aid in the development of novel therapeutics that facilitate mucosal healing and restore epithelial barrier function.

关键词： Intestinal stem cell epithelial repair Homeostasis Regeneration Selfrenewal Apoptosis

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Mucosal healing progression after acute colitis in mice

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World Journal of Gastroenterology 2019年第27期25卷 3572-3589页

作者： Sandra Vidal-Lletjós Mireille Andriamihaja Anne Blais Marta Grauso Patricia Lepage Anne-Marie Davila Claire Gaudichon Marion Leclerc Francois Blachier Annaig Lan UMR PNCA AgroParisTechINRAUniversite Paris-SaclayParis 75005France UMR MICALIS INRAUniversite Paris-SaclayJouy-en-Josas 78350France

BACKGROUND Mucosal healing has become a therapeutic goal to achieve stable remission in patients with inflammatory bowel diseases. To achieve this objective, overlapping actions of complex cellular processes, such as migration, proliferation, and differentiation, are required. These events are longitudinally and tightly controlled by numerous factors including a wide range of distinct regulatory proteins. However, the sequence of events associated with colon mucosal repair after colitis and the evolution of the luminal content characteristics during this process have been little studied.AIM To document the evolution of colon mucosal characteristics during mucosal healing using a mouse model with chemically-induced colitis.METHODS C57 BL/6 male mice were given 3.5% dextran sodium sulfate(DSS) in drinking water for 5 d. They were euthanized 2(day 7), 5(day 10), 8(day 13), and 23(day28) d after DSS removal. The colonic luminal environment and epithelial repair processes during the inflammatory flare and colitis resolution were analyzed with reference to a non-DSS treated control group, euthanized at day 0. epithelial repair events were assessed histo-morphologically in combination with functional permeability tests, expression of key inflammatory and repairing factors, and evaluation of colon mucosa-adherent microbiota composition by 16 S rRNA sequencing.RESULTS The maximal intensity of colitis was concomitant with maximal alterations of intestinal barrier function and histological damage associated with goblet cell depletion in colon mucosa. It was recorded 2 d after termination of the DSStreatment, followed by a progressive return to values similar to those of control mice. Although signs of colitis were severe(inflammatory cell infiltrate, crypt disarray, increased permeability) and associated with colonic luminal alterations(hyperosmolarity, dysbiosis, decrease in short-chain fatty acid content), epithelial healing processes were launched early during the inflammatory flare with increased gene expression of cert

关键词： Colon luminal environment Dextran sodium sulfate-induced colitis Dysbiosis epithelial repair Acute colitis

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