ArticlePurinergic signalling2009
Involvement of P2X receptors in the NAD(+)-induced rise in [Ca (2+)] (i) in human monocytes.
Article in Purinergic signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Sirtuin 6 Regulates the Activation of the ATP/Purinergic Axis in Endothelial Cells.International journal of molecular sciences · 2023Article
- Physiologic roles of P2 receptors in leukocytes.Journal of leukocyte biology · 2022Review
- Sex-related differences in human plasma NAD+/NADH levels depend on age.Bioscience reports · 2021Article
- The Extracellular NADome Modulates Immune Responses.Frontiers in immunology · 2021Review
- Perception of Damaged Self in Plants.Plant physiology · 2020Review
- Exogenous Nicotinamide Adenine Dinucleotide Induces Resistance to Citrus Canker in Citrus.Frontiers in plant science · 2018Article
- Extracellular pyridine nucleotides as immune elicitors in arabidopsis.Plant signaling & behavior · 2017Article
- A lectin receptor kinase as a potential sensor for extracellular nicotinamide adenine dinucleotide ineLife · 2017Article
- Effects of exogenous nicotinamide adenine dinucleotide (NAD+) in the rat heart are mediated by P2 purine receptors.Journal of biomedical science · 2016Article
- Effects of NAD at purine receptors in isolated blood vessels.Purinergic signalling · 2015Article
- The purinergic neurotransmitter revisited: a single substance or multiple players?Pharmacology & therapeutics · 2014Review
- Article
- P2X receptor-dependent erythrocyte damage by α-hemolysin from Escherichia coli triggers phagocytosis by THP-1 cells.Toxins · 2013Article
- Article
- Intracellular β-nicotinamide adenine dinucleotide inhibits the skeletal muscle ClC-1 chloride channel.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we show that the extracellular addition of nicotinamide adenine dinucleotide (NAD(+)) induces a transient rise in [Ca(2+)](i) in human monocytes caused by an influx of extracellular calcium. The NAD(+)-induced Ca(2+) response was prevented by adenosine triphosphate (ATP), suggesting the involvement of ATP receptors. Of the two subtypes of ATP receptors (P2X and P2Y), the P2X receptors were considered the most likely candidates. By the use of subtype preferential agonists and antagonists, we identified P2X(1), P2X(4), and P2X(7) receptors being engaged in the NAD(+)-induced rise in [Ca(2+)](i). Among the P2X receptor subtypes, the P2X(7) receptor is unique in facilitating the induction of nonselective pores that allow entry of ethidium upon stimulation with ATP. In monocytes, opening of P2X(7) receptor-dependent pores strongly depends on specific ionic conditions. Measuring pore formation in response to NAD(+), we found that NAD(+) unlike ATP lacks the ability to induce this pore-forming response. Whereas as little as 100 muM ATP was sufficient to activate the nonselective pore, NAD(+) at concentrations up to 2 mM had no effect. Taken together, these data indicate that despite similarities in the action of extracellular NAD(+) and ATP there are nucleotide-specific variations. So far, common and distinct features of the two nucleotides are only beginning to be understood.
Identifiers
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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.