Document Detail

The interaction of Bcl-2 and Bax regulates apoptosis in biliary epithelial cells of rats with obstructive jaundice.
MedLine Citation:
PMID:  10335944     Owner:  NLM     Status:  MEDLINE    
A complex molecular network controls cell homeostasis by inducing apoptosis or proliferation. The balance of Bcl-2 and Bax, members of a protein family, determines whether a cell will become immortal (Bcl-2) or will undergo apoptosis (Bax). To determine the role of Bcl-2 and Bax during proliferation of biliary epithelial cells (BEC) after bile duct ligation (BDL) and their regression after biliary decompression we induced hyperplasia of BEC by BDL in male rats. Regression of hyperplastic BEC by way of apoptosis was induced by biliary decompression through a Roux-en-Y biliodigestive anastomosis. To quantify apoptosis a modified TUNEL assay was used. Expression of Bcl-2 and Bax was visualized by immunohistochemistry and quantified stereologically. BEC increased from <1% to >20% after BDL; this increase was associated with overexpression of Bcl-2 in up to 30% of hyperplastic BEC. After biliodigestive anastomosis, apoptotic BEC increased from <0.1% to a peak of 5.4% after 1 day to reach baseline again 1 week after decompression. This was associated with de novo appearance of Bax. The interaction between Bcl-2 and Bax triggers apoptosis in BEC and acts as a cell rheostat in BEC hyperplasia and its involution after biliary decompression.
B J Stähelin; U Marti; H Zimmermann; J Reichen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Virchows Archiv : an international journal of pathology     Volume:  434     ISSN:  0945-6317     ISO Abbreviation:  Virchows Arch.     Publication Date:  1999 Apr 
Date Detail:
Created Date:  1999-06-03     Completed Date:  1999-06-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9423843     Medline TA:  Virchows Arch     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  333-9     Citation Subset:  IM    
Department of Internal Medicine, Inselspital, Berne, Switzerland.
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MeSH Terms
Anastomosis, Roux-en-Y
Bile Ducts / surgery
Bile Ducts, Intrahepatic / chemistry,  metabolism*,  pathology
Cholestasis / metabolism*,  pathology
Epithelial Cells / chemistry,  metabolism*,  pathology
Hyperplasia / pathology
Immunoenzyme Techniques
In Situ Nick-End Labeling
Liver / chemistry,  metabolism,  pathology
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-bcl-2 / metabolism*
Rats, Sprague-Dawley
bcl-2-Associated X Protein
Reg. No./Substance:
0/Bax protein, rat; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein

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