ArticleMolecular and cellular biochemistry2003
Adenosine protects against angiotensin II-induced apoptosis in rat cardiocyte cultures.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- SNHG16 accelerates the proliferation of primary cardiomyocytes by targeting miRNA-770-5p.Experimental and therapeutic medicine · 2020Article
- Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016Review
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Cardiomyocyte death induced by ischaemic/hypoxic stress is differentially affected by distinct purinergic P2 receptors.Journal of cellular and molecular medicine · 2012Article
- Ischemia-induced brain damage is enhanced in human renin and angiotensinogen double-transgenic mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2009Article
- Opposite effects of uracil and adenine nucleotides on the survival of murine cardiomyocytes.Journal of cellular and molecular medicine · 2008Article
- Adenosine protects against suicidal erythrocyte death.Pflugers Archiv : European journal of physiology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Adenosine has been found to be cardioprotective during episodes of cardiac ischemia/reperfusion through activation of the A1 and possibly A1 receptors. Therefore, we have investigated whether activation of these receptors can protect also against apoptotic death induced by angiotensin II (Ang II) in neonatal rat cardiomyocyte cultures. Exposure to Ang II (10 nM) resulted in a 3-fold increase in programmed cell death (p < 0.05). Pretreatment with the A1 adenosine receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA, 1 microM), abolished the effects of Ang II on programmed cardiomyocyte death. Moreover, exposure of cells to the A1 adenosine receptor antagonist 8-cyclopentyl- 1,3-dipropylxanthine (CPX) before pretreatment with CCPA, prevented the protective effect of the latter. Pretreatment with the A3 adenosine receptor agonist N6-(3-iodobenzyl) adenosine-5'-N-methyluronamide (IB-MECA, 0.1 microM), led to a partial decrease in apoptotic rate induced by Ang II. Exposure of myocytes to Ang II caused an immediate increase in the concentration of intracellular free Ca2+ that lasted 40-60 sec. Pretreatment of cells with CCPA or IB-MECA did not block Ang II-induced Ca2+ elevation. In conclusion, activation of adenosine A1 receptors can protect the cardiac cells from apoptosis induced by Ang II, while activation of the adenosine A3 receptors confers partial cardioprotection.
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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.