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.