Calcium signalling through nucleotide receptor P2X1 in rat portal vein myocytes

Mironneau, Jean; Coussin, Frédéric; Morel, Jean-Luc; Barbot, C.; Jeyakumar, Loice H.; Fleischer, Sidney; Mironneau, C.

doi:10.1111/j.1469-7793.2001.0339c.xd

Cited by 26 publications

(24 citation statements)

References 39 publications

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“…P2X 1 receptors appear to be principally involved in the inward current and calcium entry in rat portal vein myocytes (310). The effect of ATP is mimicked by ␣␤meATP (0.1-100 M) and, most convincingly, the inward current is not seen in cells recorded with pipettes containing an anti-P2X 1 subunit antibody.…”

Section: Smooth Musclementioning

confidence: 93%

Molecular Physiology of P2X Receptors

North

2002

Physiological Reviews

2,691

128

3,397

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P2X receptors are membrane ion channels that open in response to the binding of extracellular ATP. Seven genes in vertebrates encode P2X receptor subunits, which are 40–50% identical in amino acid sequence. Each subunit has two transmembrane domains, separated by an extracellular domain (∼280 amino acids). Channels form as multimers of several subunits. Homomeric P2X1, P2X2, P2X3, P2X4, P2X5, and P2X7 channels and heteromeric P2X2/3 and P2X1/5 channels have been most fully characterized following heterologous expression. Some agonists (e.g., αβ-methylene ATP) and antagonists [e.g., 2′,3′- O-(2,4,6-trinitrophenyl)-ATP] are strongly selective for receptors containing P2X1 and P2X3subunits. All P2X receptors are permeable to small monovalent cations; some have significant calcium or anion permeability. In many cells, activation of homomeric P2X7 receptors induces a permeability increase to larger organic cations including some fluorescent dyes and also signals to the cytoskeleton; these changes probably involve additional interacting proteins. P2X receptors are abundantly distributed, and functional responses are seen in neurons, glia, epithelia, endothelia, bone, muscle, and hemopoietic tissues. The molecular composition of native receptors is becoming understood, and some cells express more than one type of P2X receptor. On smooth muscles, P2X receptors respond to ATP released from sympathetic motor nerves (e.g., in ejaculation). On sensory nerves, they are involved in the initiation of afferent signals in several viscera (e.g., bladder, intestine) and play a key role in sensing tissue-damaging and inflammatory stimuli. Paracrine roles for ATP signaling through P2X receptors are likely in neurohypophysis, ducted glands, airway epithelia, kidney, bone, and hemopoietic tissues. In the last case, P2X7 receptor activation stimulates cytokine release by engaging intracellular signaling pathways.

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Section: Smooth Musclementioning

confidence: 93%

Molecular Physiology of P2X Receptors

North

2002

Physiological Reviews

2,691

128

3,397

View full text Add to dashboard Cite

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“…The CICR mechanism can also be activated by ionotropic P2X receptor activation in VSMC [26]. The application of 1 μmol/l αβMe-ATP, a selective activator of the P2X receptor was used to confirm the increase in CICR in HU models.…”

Section: Hu Induces Also An Increase In Cicrmentioning

confidence: 99%

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Morel

Dabertrand

Porte

et al. 2013

Pflugers Arch - Eur J Physiol

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Microgravity induces a redistribution of blood volume. Consequently, astronauts' body pressure is modified so that the upright blood pressure gradient is abolished, thereby inducing a modification in cerebral blood pressure. This effect is mimicked in the hindlimb unloaded rat model. After a duration of 8 days of unloading, Ca 2+ signals activated by depolarization and inositol-1,4,5-trisphosphate intracellular release were increased in cerebral arteries. In the presence of ryanodine and thapsigargin, the depolarization-induced Ca 2+ signals remained increased in hindlimb suspended animals, indicating that Ca 2+ influx and Ca 2+ -induced Ca 2+ release mechanism were both increased. Spontaneous Ca 2+ waves and localized Ca 2+ events were also investigated. Increases in both amplitude and frequency of spontaneous Ca 2+ waves were measured in hindlimb suspension conditions. After pharmacological segregation of Ca 2+ sparks and Ca 2+ sparklets, their kinetic parameters were characterized. Hindlimb suspension induced an increase in the frequencies of both Ca 2+ localized events, suggesting an increase of excitability. Labeling with bodipy compounds suggested that voltage-dependent Ca 2+ channels and ryanodine receptor expressions were increased. Finally, the expression of the ryanodine receptor subtype 1 (RyR1) was increased in hindlimb unloading conditions. Taken together, these results suggest that RyR1 expression and voltage-dependent Ca 2+ channels activity are the focal points of the regulation of Ca 2+ signals activated by vasoconstriction in rat cerebral arteries with an increase of the voltage-dependent Ca 2+ influx.

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“…On vascular smooth muscle cells, P2Y1, P2Y2, P2Y6, P2X1, P2X3, P2X4, P2X5 and P2X7 have been described (96)(97)(98)(99)(100)(101). Vasoconstriction is the major effect on arterial smooth muscle cells in response to ATP and UDP and is mediated by P2X and P2Y6 receptors (96,97).…”

Section: 531purinergic Receptorsmentioning

confidence: 99%

The role of purinergic signaling in the liver and in transplantation: effects of extracellular nucleotides on hepatic graft vascular injury, rejection and metabolism

Beldi

Enjyoji²,

Wu³

et al. 2008

Front Biosci

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Extracellular nucleotides (e.g. ATP, UTP, ADP) are released by activated endothelium, leukocytes and platelets within the injured vasculature and bind specific cell-surface type-2 purinergic (P2) receptors. This process drives vascular inflammation and thrombosis within grafted organs. Importantly, there are also vascular ectonucleotidases i.e. ectoenzymes that hydrolyze extracellular nucleotides in the blood to generate nucleosides (viz. adenosine). Endothelial cell NTPDase1/ CD39 has been shown to critically modulate levels of circulating nucleotides. This process tends to limit the activation of platelet and leukocyte expressed P2 receptors and also generates adenosine to reverse inflammatory events. This vascular protective CD39 activity is rapidly inhibited by oxidative reactions, such as is observed with liver ischemia reperfusion injury. In this review, we chiefly address the impact of these signaling cascades following liver transplantation. Interestingly, the hepatic vasculature, hepatocytes and all non-parenchymal cell types express several components co-ordinating the purinergic signaling response. With hepatic and vascular dysfunction, we note heightened P2-expression and alterations in ectonucleotidase expression and function that may predispose to progression of disease. In addition to documented impacts upon the vasculature during engraftment, extracellular nucleotides also have direct influences upon liver function and bile flow (both under physiological and pathological states). We have recently shown that alterations in purinergic signaling mediated by altered CD39 expression have major impacts NIH Public Access Author ManuscriptFront Biosci. Author manuscript; available in PMC 2010 June 25. Published in final edited form as:Front Biosci. ; 13: 2588-2603. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript upon hepatic metabolism, repair mechanisms, regeneration and associated immune responses. Future clinical applications in transplantation might involve new therapeutic modalities using soluble recombinant forms of CD39, altering expression of this ectonucleotidase by drugs and/or using small molecules to inhibit deleterious P2-mediated signaling while augmenting beneficial adenosine-mediated effects within the transplanted liver. KeywordsTransplantation; Liver; Purinergic Receptors; Bile; CD39; ecto-ATPase; Endothelium; Immunology; Metabolism; NTPDase; Platelet; Vasculature; Review INTRODUCTIONPurinergic signaling comprises release of extracellular nucleotides, stimulation of purinergic receptors and the modulation of nucleotide levels by ectoenzymes. Over the past decade, many advances have been made in the study of purinergic receptors and the regulation of extracellular nucleotide concentrations (1). It is now generally accepted that extracellular nucleotides (e.g. ATP, UTP, ADP), and the derivative nucleosides (e.g. adenosine from ATP), are released in a regulated manner by cells to provide the primary components for purinergic responses (2). Specific nucleo...

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Calcium signalling through nucleotide receptor P2X1 in rat portal vein myocytes

Cited by 26 publications

References 39 publications

Molecular Physiology of P2X Receptors

Molecular Physiology of P2X Receptors

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

The role of purinergic signaling in the liver and in transplantation: effects of extracellular nucleotides on hepatic graft vascular injury, rejection and metabolism

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