Glial Cell Line-Derived Neurotrophic Factor, S-100 Protein and Synaptophysin Expression in Biliary Atresia Gallbladder Tissue
10.5223/pghn.2021.24.2.173
- Author:
Semra GÜRÜNLÜOĞLU
1
;
Canan CERAN
;
Kubilay GÜRÜNLÜOĞLU
;
Alper KOÇBIYIK
;
Mehmet GÜL
;
Turan YILDIZ
;
Harika Gözükara BAĞ
;
Semir GÜL
;
Aytaç TAŞÇI
;
Ercan BAYRAKÇI
;
Necmettin AKPINAR
;
Ecem Serbest ÇIN
;
Hasan ATEŞ
;
Mehmet DEMIRCAN
Author Information
1. Department of Pathology Malatya Education and Research Hospital, Pathology Laboratory, Malatya, Turkey
- Publication Type:Original Article
- From:Pediatric Gastroenterology, Hepatology & Nutrition
2021;24(2):173-186
- CountryRepublic of Korea
- Language:English
-
Abstract:
Purpose:Biliary atresia (BA) is a disease that manifests as jaundice after birth and leads to progressive destruction of the ductal system in the liver. The aim of this study was to investigate histopathological changes and immunohistochemically examine the expression of glial cell line-derived neurotrophic factor (GDNF), synaptophysin, and S-100 protein in the gallbladder of BA patients.
Methods:The study included a BA group of 29 patients and a control group of 41 children with cholecystectomy. Gallbladder tissue removed during surgery was obtained and examined immunohistochemically and histopathologically. Tissue samples of both groups were immunohistochemically assessed in terms of GDNF, S-100 protein, and synaptophysin expression. Expression was classified as present or absent. Inflammatory activity assessment with hematoxylin and eosin staining and fibrosis assessment with Masson's trichrome staining were performed for tissue sample sections of both groups.
Results:Ganglion cells were not present in gallbladder tissue samples of the BA group.Immunohistochemically, GDNF, synaptophysin, and S-100 expression was not detected in the BA group. Histopathological examination revealed more frequent fibrosis and slightly higher inflammatory activity in the BA than in the control group.
Conclusion:We speculate that GDNF expression will no longer continue in this region, when the damage caused by inflammation of the extrahepatic bile ducts reaches a critical threshold. The study's findings may represent a missing link in the chain of events forming the etiology of BA and may be helpful in its diagnosis.
