Necroptosis in biliary atresia of the liver.
Biliary atresia
Cell death
Cholangiocytes
Congenital biliary dilation
Immunohistochemistry
Liver
Necroptosis
Phosphorylated mixed lineage kinase domain-like
Journal
Medical molecular morphology
ISSN: 1860-1499
Titre abrégé: Med Mol Morphol
Pays: Japan
ID NLM: 101239023
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
25
12
2020
accepted:
26
04
2021
pubmed:
24
6
2021
medline:
15
1
2022
entrez:
23
6
2021
Statut:
ppublish
Résumé
Biliary atresia (BA) is characterized by the occlusion of extrahepatic bile ducts due to sclerosing inflammation. Necroptosis is a recently characterized form of programmed cell death but has not been examined in BA. We, therefore, explored the potential involvement of necroptosis in the pathogenesis of BA by evaluating the correlation between necroptosis-related factors and clinicopathological features of BA patients. We studied liver biopsy specimens of 59 patients with BA and 30 with congenital biliary dilatation (CBD). We also evaluated 14 surgical BA cases, who eventually underwent liver transplantation and 9 normal liver from neonates and infants obtained at autopsy. Necroptosis-related factors including toll-like receptor 3 (TLR3), receptor-interacting protein kinase1 (RIP1), receptor-interacting protein kinase3 (RIP3), mixed lineage kinase domain-like (MLKL), and phosphorylated mixed lineage kinase domain-like (pMLKL) in these liver specimens were immunolocalized. TLR3, RIP1, MLKL in the intrahepatic cholangiocytes was significantly higher in BA than CBD. pMLKL immunoreactivity was significantly greater at an earlier age of BA patients. The native liver survival period was significantly prolonged in the high RIP3 group. The low RIP3 status could serve as an adverse clinical prognostic factor for the native liver survival among the necroptosis-related factors examined in this study.
Identifiants
pubmed: 34159444
doi: 10.1007/s00795-021-00289-3
pii: 10.1007/s00795-021-00289-3
doi:
Substances chimiques
Protein Kinases
EC 2.7.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
305-315Informations de copyright
© 2021. The Japanese Society for Clinical Molecular Morphology.
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