Supported by the National Medical Research Council (NMRC) Grant (R183-000-095-213).
Altered CD38 expression in thioacetamide-induced rat model of liver cirrhosis
Version of Record online: 3 OCT 2005
Volume 25, Issue 6, pages 1233–1242, December 2005
How to Cite
Gan, B. H., Ng, G. L., Bay, B. H. and Chang, C. F. (2005), Altered CD38 expression in thioacetamide-induced rat model of liver cirrhosis. Liver International, 25: 1233–1242. doi: 10.1111/j.1478-3231.2005.01173.x
- Issue online: 11 NOV 2005
- Version of Record online: 3 OCT 2005
- Received 4 February 2005, accepted 15 June 2005
- ADP-ribosyl cyclase;
- cycling assay;
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.