| Literature DB >> 27899277 |
Eunyoung Tak1, Dong-Hwan Jung2, Seok-Hwan Kim2, Gil-Chun Park2, Dae Young Jun1, Jooyoung Lee1, Bo-Hyun Jung3, Varvara A Kirchner4, Shin Hwang2, Gi-Won Song5, Sung-Gyu Lee2.
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)-1α, 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.Entities:
Keywords: Acute liver failure; CD39; CD73; HIF-1α
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Year: 2016 PMID： 27899277 DOI： 10.1016/j.taap.2016.11.016
Source DB: PubMed Journal: Toxicol Appl Pharmacol ISSN： 0041-008X Impact factor: 4.219