ArticleExperimental cell research1998
Induction of apoptosis in cardiac myocytes by an A3 adenosine receptor agonist.
Article in Experimental cell research, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 94 citations in OpenAlex.
- Role of Adenosine and Purinergic Receptors in Myocardial Infarction: Focus on Different Signal Transduction Pathways.Biomedicines · 2021Review
- Identification of A3 adenosine receptor agonists as novel non-narcotic analgesics.British journal of pharmacology · 2016Review
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Adenosine receptors and renal ischaemia reperfusion injury.Acta physiologica (Oxford, England) · 2015Review
- P2Y2 receptor agonist with enhanced stability protects the heart from ischemic damage in vitro and in vivo.Purinergic signalling · 2013Article
- Effects of synthetic A3 adenosine receptor agonists on cell proliferation and viability are receptor independent at micromolar concentrations.Journal of physiology and biochemistry · 2013Article
- Toward on-chip, in-cell recordings from cultured cardiomyocytes by arrays of gold mushroom-shaped microelectrodes.Frontiers in neuroengineering · 2012Article
- Adenosine and protection from acute kidney injury.Current opinion in nephrology and hypertension · 2012Review
- Involvement of UTP in protection of cardiomyocytes from hypoxic stress.Canadian journal of physiology and pharmacology · 2009Article
- Transplantation of genetically engineered cardiac fibroblasts producing recombinant human erythropoietin to repair the infarcted myocardium.Fibrogenesis & tissue repair · 2008Article
- The Anti-Cancer Effect of AImmunology, endocrine & metabolic agents in medicinal chemistry · 2007Article
- Modulation of the Akt/Ras/Raf/MEK/ERK pathway by A₃ adenosine receptor.Purinergic signalling · 2006Article
- Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.Biochemical pharmacology · 2006Article
- Delta-9-tetrahydrocannabinol protects cardiac cells from hypoxia via CB2 receptor activation and nitric oxide production.Molecular and cellular biochemistry · 2006Article
- Involvement of uracil nucleotides in protection of cardiomyocytes from hypoxic stress.Biochemical pharmacology · 2005Article
- Extracellular ATP and adenosine induce cell apoptosis of human hepatoma Li-7A cells via the A3 adenosine receptor.British journal of pharmacology · 2003Article
- Adenosine protects against angiotensin II-induced apoptosis in rat cardiocyte cultures.Molecular and cellular biochemistry · 2003Article
- A3 adenosine receptors in human astrocytoma cells: agonist-mediated desensitization, internalization, and down-regulation.Molecular pharmacology · 2002Article
- p53-Independent induction of Fas and apoptosis in leukemic cells by an adenosine derivative, Cl-IB-MECA.Biochemical pharmacology · 2002Article
- Insights into the cardioprotective function of adenosine A(1) and A(3) receptors.Experimental and clinical cardiology · 2002Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
The effects of the selective adenosine (ADO) A3 receptor agonist IB-MECA (N6-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide) on cultured newborn rat cardiomyocytes were examined in comparison with ADO, the ADO A1 receptor-selective agonist R-PIA (N6-R-phenylisopropyladenosine), or the ADO A3 selective antagonist MRS 1191 (3-ethyl-5-benzyl-2-methyl-6-phenyl-4-phenylethynyl-1, 4-(+/-)-dihydropyridine-3,5 dicarboxylate), using digital image analysis of Feulgen-stained nuclei. At high concentration, IB-MECA (>/=10 microM ) and ADO (200 microM) induced apoptosis; however, R-PIA or MRS 1191 did not have any detectable effects on cardiac cells. In addition, DNA breaks in cardiomyocytes undergoing apoptosis following treatment by IB-MECA were identified in situ using the nick end labeling of DNA ("TUNEL"-like) assay. In the presence of >/=10 microM IB-MECA, disorder in the contraction waves appeared, and a decrease in the frequency of beats was observed. Analysis with light microscopy revealed that the number of contracting cells decreased in a concentration-dependent manner. The A3 receptor agonist IB-MECA caused an increase in intracellular free calcium concentration ([Ca2+]i). The drug produced a rapid rise followed by a sustained increase in [Ca2+]i, which lasted for 40-60 s. Finally, cessation of beating and Ca2+ transients were observed. Full recovery of contractile activity and rhythmical Ca2+ transients were observed 15-20 min after IB-MECA treatment. The induction of apoptosis in the cardiocytes by IB-MECA led to the appearance of features of apoptotic nuclei: the onset of condensation, compacting, and margination of nuclear chromatin. These effects were accompanied by the disintegration of the structural framework of the nucleus and nuclear breakdown. The results suggest that activation of the A3 adenosine receptor may participate in the process of apoptosis in cardiomyocytes.
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