Prominin-1 Promotes Biliary Fibrosis Associated With Biliary Atresia.
AC133 Antigen
/ genetics
Animals
Animals, Newborn
Bile Duct Diseases
/ genetics
Biliary Atresia
/ genetics
Biopsy, Needle
Cells, Cultured
Disease Models, Animal
Fibrosis
/ pathology
Gene Expression Regulation
Humans
Immunohistochemistry
Mice
Mice, Knockout
Mutation
/ genetics
Random Allocation
Risk Assessment
Rotavirus
/ pathogenicity
Rotavirus Infections
/ pathology
Sensitivity and Specificity
Transcription Factors
/ metabolism
Journal
Hepatology (Baltimore, Md.)
ISSN: 1527-3350
Titre abrégé: Hepatology
Pays: United States
ID NLM: 8302946
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
29
06
2018
accepted:
29
01
2019
pubmed:
7
2
2019
medline:
17
6
2020
entrez:
7
2
2019
Statut:
ppublish
Résumé
In patients with biliary atresia (BA), the extent of intrahepatic biliary fibrosis negatively correlates with successful surgical bypass of the congenital cholangiopathy as well as subsequent transplant-free survival. We recently linked the expansion of a population of prominin-1 (Prom1)-expressing hepatic progenitor cells to biliary fibrogenesis. Herein, we hypothesized that Prom1-expressing progenitor cells play a role in BA-associated fibrosis. Rhesus rotavirus (RRV)-mediated experimental BA was induced in newborn mice homozygous for the transgene Prom1
Identifiants
pubmed: 30723921
doi: 10.1002/hep.30550
pmc: PMC6541523
mid: NIHMS1030700
doi:
Substances chimiques
AC133 Antigen
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2586-2597Subventions
Organisme : NIDDK NIH HHS
ID : U01 DK084538
Pays : United States
Informations de copyright
© 2019 by the American Association for the Study of Liver Diseases.
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