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Altered CD38 expression in thioacetamide-induced rat model of liver cirrhosis


  • Supported by the National Medical Research Council (NMRC) Grant (R183-000-095-213).

Chan Fong Chang, Department of Biochemistry, Faculty of Medicine, National University of Singapore, 8, Medical Drive, Singapore 117597, Singapore.
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Abstract: Background: Cirrhosis is a gradually developing, chronic disease which involves the whole liver. Here, we have shown that CD38 undergoes altered expression upon thioacetamide-induced cirrhosis in rats. CD38 is a type II transmembrane glycoprotein that exhibits ADP-ribosyl cyclase and cADPR hydrolase activities. In this study, the gene and protein expressions of CD38 were investigated in a thioacetamide-induced rat model of cirrhosis.

Methods: CD38 expression was studied by using real-time RT-PCR, immunohistochemistry, and immunoblotting. cADPR content in liver was measured using cycling assay.

Results: There was a significant increase in CD38 mRNA and protein expressions as well as ADP-ribosyl cyclase activity in cirrhotic liver compared to the control liver. cADPR level was found to be modestly but significantly augmented in cirrhotic liver.

Conclusions: These results raised the possibility that altered CD38 expression and a concomitant elevation of the enzymatic activity as well as cADPR may be involved in the pathogenesis of liver cirrhosis.

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