FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2008266983> ?p ?o ?g. }

• W2008266983 endingPage "1412" @default.
• W2008266983 startingPage "1401" @default.
• W2008266983 abstract "Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of bile duct integrity in mice challenged with biliary-type liver injury. Vdr(-/-) mice subjected to bile duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice. Adaptation to cholestasis, ascertained by expression of genes involved in bile acid metabolism and tissue repair, was limited in Vdr(-/-) BDL mice. Furthermore, evaluation of Vdr(-/-) BDL mouse liver tissue sections indicated altered E-cadherin staining associated with increased bile duct rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr(-/-) mice subjected to BDL compared to wildtype BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the epidermal growth factor receptor (EGFR) pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells.Biliary-type liver injury is exacerbated in Vdr(-/-) mice by limited adaptive response and increased bile duct rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes bile duct integrity in the setting of biliary-type liver injury." @default.
• W2008266983 created "2016-06-24" @default.
• W2008266983 creator A5008398995 @default.
• W2008266983 creator A5041662580 @default.
• W2008266983 creator A5043299615 @default.
• W2008266983 creator A5047380758 @default.
• W2008266983 creator A5060912987 @default.
• W2008266983 creator A5067010874 @default.
• W2008266983 creator A5074609427 @default.
• W2008266983 creator A5075826396 @default.
• W2008266983 creator A5076013292 @default.
• W2008266983 creator A5078313558 @default.
• W2008266983 creator A5082707335 @default.
• W2008266983 creator A5087041626 @default.
• W2008266983 date "2013-09-06" @default.
• W2008266983 modified "2023-10-12" @default.
• W2008266983 title "Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice" @default.
• W2008266983 cites W1506285409 @default.
• W2008266983 cites W1971013426 @default.
• W2008266983 cites W1978346927 @default.
• W2008266983 cites W1979266334 @default.
• W2008266983 cites W1982260172 @default.
• W2008266983 cites W1988779510 @default.
• W2008266983 cites W1993561986 @default.
• W2008266983 cites W1993882745 @default.
• W2008266983 cites W1995636102 @default.
• W2008266983 cites W2000747270 @default.
• W2008266983 cites W2002121467 @default.
• W2008266983 cites W2013845701 @default.
• W2008266983 cites W2015624008 @default.
• W2008266983 cites W2018809127 @default.
• W2008266983 cites W2021754267 @default.
• W2008266983 cites W2044213834 @default.
• W2008266983 cites W2046306450 @default.
• W2008266983 cites W2050495493 @default.
• W2008266983 cites W2070347103 @default.
• W2008266983 cites W2074274895 @default.
• W2008266983 cites W2077767424 @default.
• W2008266983 cites W2081476109 @default.
• W2008266983 cites W2087333134 @default.
• W2008266983 cites W2088811320 @default.
• W2008266983 cites W2092031603 @default.
• W2008266983 cites W2098453507 @default.
• W2008266983 cites W2107248034 @default.
• W2008266983 cites W2107746069 @default.
• W2008266983 cites W2108872477 @default.
• W2008266983 cites W2111567870 @default.
• W2008266983 cites W2118263188 @default.
• W2008266983 cites W2122341732 @default.
• W2008266983 cites W2128245496 @default.
• W2008266983 cites W2138153315 @default.
• W2008266983 cites W2139294932 @default.
• W2008266983 cites W2140403377 @default.
• W2008266983 cites W2141845531 @default.
• W2008266983 cites W2145336541 @default.
• W2008266983 cites W2146711122 @default.
• W2008266983 cites W2156827860 @default.
• W2008266983 cites W2164906049 @default.
• W2008266983 cites W2167093722 @default.
• W2008266983 doi "https://doi.org/10.1002/hep.26453" @default.
• W2008266983 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4286017" @default.
• W2008266983 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23696511" @default.
• W2008266983 hasPublicationYear "2013" @default.
• W2008266983 type Work @default.
• W2008266983 sameAs 2008266983 @default.
• W2008266983 citedByCount "39" @default.
• W2008266983 countsByYear W20082669832014 @default.
• W2008266983 countsByYear W20082669832015 @default.
• W2008266983 countsByYear W20082669832016 @default.
• W2008266983 countsByYear W20082669832017 @default.
• W2008266983 countsByYear W20082669832018 @default.
• W2008266983 countsByYear W20082669832019 @default.
• W2008266983 countsByYear W20082669832020 @default.
• W2008266983 countsByYear W20082669832021 @default.
• W2008266983 countsByYear W20082669832022 @default.
• W2008266983 countsByYear W20082669832023 @default.
• W2008266983 crossrefType "journal-article" @default.
• W2008266983 hasAuthorship W2008266983A5008398995 @default.
• W2008266983 hasAuthorship W2008266983A5041662580 @default.
• W2008266983 hasAuthorship W2008266983A5043299615 @default.
• W2008266983 hasAuthorship W2008266983A5047380758 @default.
• W2008266983 hasAuthorship W2008266983A5060912987 @default.
• W2008266983 hasAuthorship W2008266983A5067010874 @default.
• W2008266983 hasAuthorship W2008266983A5074609427 @default.
• W2008266983 hasAuthorship W2008266983A5075826396 @default.
• W2008266983 hasAuthorship W2008266983A5076013292 @default.
• W2008266983 hasAuthorship W2008266983A5078313558 @default.
• W2008266983 hasAuthorship W2008266983A5082707335 @default.
• W2008266983 hasAuthorship W2008266983A5087041626 @default.
• W2008266983 hasBestOaLocation W20082669834 @default.
• W2008266983 hasConcept C124490489 @default.
• W2008266983 hasConcept C126322002 @default.
• W2008266983 hasConcept C134018914 @default.
• W2008266983 hasConcept C1491633281 @default.
• W2008266983 hasConcept C149402561 @default.
• W2008266983 hasConcept C179639408 @default.
• W2008266983 hasConcept C2776637226 @default.
• W2008266983 hasConcept C2778593092 @default.

• next