Skip to main content
 
Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
Stanford Health Care

Protective role of hypoxia-inducible factor-1a-dependent CD39 and CD73 in fulminant acute liver failure.

Protective role of hypoxia-inducible factor-1a-dependent CD39 and CD73 in fulminant acute liver failure. Toxicology and applied pharmacology Tak, E., Jung, D. H., Kim, S. H., Park, G. C., Jun, D. Y., Lee, J., Jung, B. H., Kirchner, V. A., Hwang, S., Song, G. W., Lee, S. G. 2017; 314: 72-81

Abstract

Acute liver failure (ALF) is a severe life-threatening disease which usually arises in patients with-irreversible liver illnesses. Although human ectonucleotide triphosphate diphosphohydrolase-1, E-NTPDase1 (CD39) and ecto-5'-nucleotidase, Ecto5'NTase (CD73) are known to protect tissues from ALF, the expression and function of CD39 and CD73 during ALF are currently not fully investigated. We tested whether CD39 and CD73 are upregulated by hypoxia inducible factor (HIF)-1a, and improve ischemic tolerance to ALF. To test our hypothesis, liver biopsies were obtained and we found that CD39 and CD73 mRNA and proteins from human specimens were dramatically elevated in ALF. We investigated that induction of CD39 and CD73 in ALF-related with wild type mice. In contrast, deletion of cd39 and cd73 mice has severe ALF. In this study, we concluded that CD39 and CD73 are molecular targets for the development of drugs for ALF patients care.

View details for DOI 10.1016/j.taap.2016.11.016

View details for PubMedID 27899277