Expression of Bax, Bcl-xL and Bcl-2 proteins in relation to grade of inflammation and stage of fibrosis in chronic hepatitis C

Aims:  To determine the expression of regulators of apoptosis in chronic hepatitis C. Methods and results:  Expression of Bax, Bcl‐xL and Bcl‐2 proteins was assessed immunohistochemically in liver biopsy specimens obtained from 89 adults with chronic hepatitis C. Expression of Bax in hepatocytes cor...

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Published in:Histopathology Vol. 50; no. 7; pp. 928 - 935
Main Authors: Piekarska, A, Kubiak, R, Szymczak, W, Piekarski, J
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01-06-2007
Blackwell
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Summary:Aims:  To determine the expression of regulators of apoptosis in chronic hepatitis C. Methods and results:  Expression of Bax, Bcl‐xL and Bcl‐2 proteins was assessed immunohistochemically in liver biopsy specimens obtained from 89 adults with chronic hepatitis C. Expression of Bax in hepatocytes correlated inversely with grade of inflammation (P < 0.001) and stage of fibrosis (P = 0.011), classified according to the Scheuer score; expression of Bcl‐xL in hepatocytes did not correlate with grade of inflammation (P = 0.106) or stage of fibrosis (P = 0.078); maximum Bcl‐xL expression was observed in grade 3 inflammation and stage 4 fibrosis. Expression of Bcl‐2 protein in hepatocytes was present in only two cases (both with advanced disease); the expression of Bcl‐2 protein in interlobular bile duct epithelial cells correlated with the grade of inflammation (P = 0.018), but not with stage of fibrosis (P = 0.154). The expression of Bcl‐2 protein in lymphoid cells infiltrating portal zones and lobules did not correlate with grade of inflammation (P = 0.113) or stage of fibrosis (P = 0.815). Conclusion:  Major differences in expression of studied proteins were observed in relation to grade of inflammation and stage of fibrosis in chronic hepatitis C.
Bibliography:ark:/67375/WNG-PCN27RRK-Z
istex:0CE8AA1DA5BE6343F81491139526FE494BEBF301
ArticleID:HIS2697
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0309-0167
1365-2559
DOI:10.1111/j.1365-2559.2007.02697.x