ArticleJournal of immunology (Baltimore, Md. : 1950)2010
SP1-dependent induction of CD39 facilitates hepatic ischemic preconditioning.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
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Who cites it
83 citing papers in PubMed, 127 citations in OpenAlex.
- Neutrophil-T cell cross talk in noninfectious liver diseases.American journal of physiology. Gastrointestinal and liver physiology · 2026Review
- Potential of Adora2b as an immunotherapeutic target for gastric cancer.Frontiers in immunology · 2025Review
- Purinergic signaling and cholangiocyte regeneration: a new frontier in ischemic liver injury.Frontiers in transplantation · 2025Review
- Nucleotide polymorphism-based study utilizes human plasma liposomes to discover potential therapeutic targets for intervertebral disc disease.Frontiers in endocrinology · 2024Article
- Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering ARespiratory research · 2023Article
- Circulating Ectonucleotidases Signal Impaired Myocardial Perfusion at Rest and Stress.Journal of the American Heart Association · 2023Article
- Review
- Adenosine, bridging chronic inflammation and tumor growth.Frontiers in immunology · 2023Review
- The hypoxic tissue microenvironment as a driver of mucosal inflammatory resolution.Frontiers in immunology · 2023Review
- The resurgence of the Adora2b receptor as an immunotherapeutic target in pancreatic cancer.Frontiers in immunology · 2023Review
- Ectonucleoside triphosphate diphosphohydrolase-1 (CD39) impacts TGF-β1 responses: insights into cardiac fibrosis and function following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- The Hypoxia-Adenosine Link during Myocardial Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Alternative adenosine Receptor activation: The netrin-Adora2b link.Frontiers in pharmacology · 2022Review
- Purinergic and Adenosinergic Signaling in Pancreatobiliary Diseases.Frontiers in physiology · 2022Review
- Role of Purinergic Signalling in Endothelial Dysfunction and Thrombo-Inflammation in Ischaemic Stroke and Cerebral Small Vessel Disease.Biomolecules · 2021Review
- Targeting ectonucleotidases to treat inflammation and halt cancer development in the gut.Biochemical pharmacology · 2021Review
- Hyperhomocysteinemia and Cardiovascular Disease: Is the Adenosinergic System the Missing Link?International journal of molecular sciences · 2021Review
- Skewed CD39/CD73/adenosine pathway contributes to B-cell hyperactivation and disease progression in patients with chronic hepatitis B.Gastroenterology report · 2021Article
- Purinergic signalling in liver diseases: Pathological functions and therapeutic opportunities.JHEP reports : innovation in hepatology · 2020Review
- Endogenous antisense RNA curbs CD39 expression in Crohn's disease.Nature communications · 2020Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischemia/reperfusion injury (IRI) of the liver is an important cause of hepatic dysfunction. Ischemic preconditioning (IP) is associated with adenosine-mediated tissue protection from subsequent IRI. Extracellular nucleotides (e.g., ATP) represent the main source for extracellular adenosine. Therefore, we hypothesized that phosphohydrolysis of ATP/ADP via the ectonucleoside triphosphate diphosphohydrolase-1 (CD39), conversion of ATP/ADP to AMP, mediates IP-dependent liver protection. We found that hepatic IP was associated with significant induction of CD39 transcript, heightened protein expression, and improved outcomes after IRI. Targeted gene deletion or pharmacological inhibition of CD39 abolished hepatoprotection by IP as measured by serum markers of liver injury or histology. Therapeutic studies to mimic IP with i.p. apyrase (a soluble ectonucleoside triphosphate diphosphohydrolase, NTPDase) in the absence of IP attenuated hepatic injury after IRI. In additional in vivo studies, small interfering RNA treatment was used to achieve repression of the transcription factor Sp1, known to be implicated in CD39 transcriptional regulation. In fact, Sp1 small interfering RNA treatment was associated with attenuated CD39 induction and increased hepatic injury in vivo. Our data suggest a Sp1-dependent regulatory pathway for CD39 during hepatic IP. These studies reveal a novel role of CD39 in hepatic protection and suggest soluble apyrase for the treatment of liver ischemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.