دورية أكاديمية
Prominin-1 promotes restitution of the murineMAQ:Editorial Office/AASLD: Please indicate if a visual abstract will be forthcoming for this article. extrahepatic biliary luminal epithelium following cholestatic liver injury
العنوان: | Prominin-1 promotes restitution of the murineMAQ:Editorial Office/AASLD: Please indicate if a visual abstract will be forthcoming for this article. extrahepatic biliary luminal epithelium following cholestatic liver injury |
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المؤلفون: | Allen Zhong, Celia Short, Jiabo Xu, G. Esteban Fernandez, Nicolas Malkoff, Nicolas Noriega, Theresa Yeo, Larry Wang, Nirmala Mavila, Kinji Asahina, Kasper S. Wang |
المصدر: | Hepatology Communications, Vol 7, Iss 2, Pp e0018-e0018 (2023) |
بيانات النشر: | Wolters Kluwer Health/LWW, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Diseases of the digestive system. Gastroenterology |
مصطلحات موضوعية: | Diseases of the digestive system. Gastroenterology, RC799-869 |
الوصف: | Background and Aims:. Restitution of the extrahepatic biliary luminal epithelium in cholangiopathies is poorly understood. Prominin-1 (Prom1) is a key component of epithelial ciliary body of stem/progenitor cells. Given that intrahepatic Prom1-expressing progenitor cells undergo cholangiocyte differentiation, we hypothesized that Prom1 may promote restitution of the extrahepatic bile duct (EHBD) epithelium following injury. Approach and Results:. Utilizing various murine biliary injury models, we identified Prom1-expressing cells in the peribiliary glands of the EHBD. These Prom1-expressing cells are progenitor cells which give rise to cholangiocytes as part of the normal maintenance of the EHBD epithelium. Following injury, these cells proliferate significantly more rapidly to re-populate the biliary luminal epithelium. Null mutation of Prom1 leads to significantly >10-fold dilated peribiliary glands following rhesus rotavirus–mediated biliary injury. Cultured organoids derived from Prom1 knockout mice are comprised of biliary progenitor cells with altered apical-basal cellular polarity, significantly fewer and shorter cilia, and decreased organoid proliferation dynamics consistent with impaired cell motility. Conclusions:. We, therefore, conclude that Prom1 is involved in biliary epithelial restitution following biliary injury in part through its role in supporting cell polarity. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2471-254X 00000000 |
Relation: | http://journals.lww.com/10.1097/HC9.0000000000000018; https://doaj.org/toc/2471-254X |
DOI: | 10.1097/HC9.0000000000000018 |
URL الوصول: | https://doaj.org/article/909ab46dd7434b64b57f08a48c3dd368 |
رقم الأكسشن: | edsdoj.909ab46dd7434b64b57f08a48c3dd368 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 2471254X 00000000 |
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DOI: | 10.1097/HC9.0000000000000018 |