ArticlePflugers Archiv : European journal of physiology2013
P2X receptor stimulation amplifies complement-induced haemolysis.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Purinergic Receptor Antagonists Inhibit Hemolysis Induced byPathogens (Basel, Switzerland) · 2024Article
- The Pleiotropic Role of Extracellular ATP in Myocardial Remodelling.Molecules (Basel, Switzerland) · 2023Review
- P2RX7 at the Host-Pathogen Interface of Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2021Review
- Prevention of P2 Receptor-Dependent Thrombocyte Activation by Pore-Forming Bacterial Toxins Improves Outcome in A Murine Model of Urosepsis.International journal of molecular sciences · 2020Article
- Erythrocyte P2XCritical care (London, England) · 2018Article
- P2X-Receptor Antagonists Inhibit the Interaction of S. aureus Hemolysin A with Membranes.Toxins · 2017Article
- Loop Diuretics Diminish Hemolysis Induced by α-Hemolysin from Escherichia coli.The Journal of membrane biology · 2017Article
- P2XFrontiers in cellular and infection microbiology · 2017Article
- Inhibition of P2X Receptors Protects Human Monocytes against Damage by Leukotoxin from Aggregatibacter actinomycetemcomitans and α-Hemolysin from Escherichia coli.Infection and immunity · 2016Article
- Blood cells: an historical account of the roles of purinergic signalling.Purinergic signalling · 2015Review
- [Ca2+]i Oscillations and IL-6 Release Induced by α-Hemolysin from Escherichia coli Require P2 Receptor Activation in Renal Epithelia.The Journal of biological chemistry · 2015Article
- P2X and P2Y receptor signaling in red blood cells.Frontiers in molecular biosciences · 2015Review
- Bacterial RTX toxins allow acute ATP release from human erythrocytes directly through the toxin pore.The Journal of biological chemistry · 2014Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the complement system evokes cell damage by insertion of membrane attack complexes, which constitute the basis of the pathogenesis of various haemolytic disorders. Recently, we found that haemolysis caused by other types of membrane pore-forming proteins such as α-haemolysin (HlyA) from Escherichia coli, α-toxin from Staphylococcus aureus and leukotoxin from Aggregatibacter actinomycetemcomitans inflict their cytotoxic effects through P2 receptor activation. Here we show that similar to haemolysis induced by HlyA, leukotoxin and α-toxin, complement-induced haemolysis is amplified through ATP release and subsequent P2 receptor activation. Similar results were found both in murine, sensitised ovine and human erythrocytes, with either human plasma or guinea pig serum as complement donors. Non-selective P2 antagonists (PPADS and suramin) concentration-dependently inhibited complement-induced haemolysis. More specific P2 receptor antagonists imply that P2X1 and P2X7 are the main receptors involved in this response. Moreover, complement activation produces a sustained increase in [Ca(2+)]i, which initially triggers significant erythrocyte shrinkage, most likely mediated by KCa3.1-dependent K(+) efflux. These results indicate that complement, similar to HlyA and α-toxin, requires purinergic signalling for full haemolysis and that activation of erythrocyte volume regulation protracts the process. This finding points to several new pathways to interfere with haemolytic diseases and implies that P2 receptor antagonists potentially can be used to prevent intravascular haemolysis.
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