Postjunctional ATP release mediated by stimulation of P2x-purinoceptors

Katsuragi, Takeshi; Tokunaga, Takeo; Ogawa, Shusuke; Soejima, Osamu; Sato, Chiemi; Furukawa, Tatsuo

doi:10.1016/s0021-5198(19)59966-8

Cited by 2 publications

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“…ATP is also stored in red blood cells (RBC) from which it is released under conditions of imbalance between O 2 supply and O 2 demand ( 81 – 84 ). In addition, several biologic substances as well as increased blood flow can induce the release of ATP from vascular endothelial cells ( 77 , 85 – 88 ) and smooth muscle cells ( 89 , 90 ). Other ATPs release stimuli and cellular sources including mechanical deformation of cells, ischemic cells, immune cells, and necrotic/apoptotic cells ( 23 , 91 – 94 ).…”

Section: Introductionmentioning

confidence: 99%

Degranulation of human mast cells: modulation by P2 receptors’ agonists

Schulman,

Nishi,

Pelleg

2023

Front. Immunol.

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Since the late 1970s, there has been an alarming increase in the incidence of asthma and its morbidity and mortality. Acute obstruction and inflammation of allergic asthmatic airways are frequently caused by inhalation of exogenous substances such as allergens cross-linking IgE receptors expressed on the surface of the human lung mast cells (HLMC). The degree of constriction of human airways produced by identical amounts of inhaled allergens may vary from day to day and even hour to hour. Endogenous factors in the human mast cell (HMC)’s microenvironment during allergen exposure may markedly modulate the degranulation response. An increase in allergic responsiveness may significantly enhance bronchoconstriction and breathlessness. This review focuses on the role that the ubiquitous endogenous purine nucleotide, extracellular adenosine 5’-triphosphate (ATP), which is a component of the damage-associated molecular patterns, plays in mast cells’ physiology. ATP activates P2 purinergic cell-surface receptors (P2R) to trigger signaling cascades resulting in heightened inflammatory responses. ATP is the most potent enhancer of IgE-mediated HLMC degranulation described to date. Current knowledge of ATP as it relates to targeted receptor(s) on HMC along with most recent studies exploring HMC post-receptor activation pathways are discussed. In addition, the reviewed studies may explain why brief, minimal exposures to allergens (e.g., dust, cat, mouse, and grass) can unpredictably lead to intense clinical reactions. Furthermore, potential therapeutic approaches targeting ATP-related enhancement of allergic reactions are presented.

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Section: Introductionmentioning

confidence: 99%

Degranulation of human mast cells: modulation by P2 receptors’ agonists

Schulman,

Nishi,

Pelleg

2023

Front. Immunol.

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ATP release and contraction mediated by different P2‐receptor subtypes in guinea‐pig ileal smooth muscle

Matsuo

Katsuragi

Fujiki

et al. 1997

British J Pharmacology

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1 The present study was addressed to clarify the subtypes of P2-purinoceptor involved in ATP release and contraction evoked by a,b-methylene ATP (a,b-mATP) and other P2-agonists in guinea-pig ileum. 2 a,b-mATP 100 mM produced a transient and steep contraction followed by ATP release from tissue segments. These maximum responses appeared with di erent time-courses and their ED 50 values were 5 and 25 mM, respectively. The maximum release of ATP by a,b-mATP was markedly reduced by 250 mM suramin, 30 mM pyridoxal-phosphate-6-azophenyl-2',5'-disulphonic acid (PPADS) and 30 mM reactive blue 2 (RB-2), P2-receptor antagonists. However, the contractile response was inhibited by suramin, tetrodotoxin and atropine, but not by PPADS and RB-2. 3 Although the contraction caused by a,b-mATP was strongly diminished by Ca 2+ -removal and nifedipine, and also by tetrodotoxin and atropine at 0.3 mM, the release of ATP was virtually una ected by these procedures. 4 UTP, b,g-methylene ATP (b,g-mATP) and ADP at 100 mM elicited a moderate release of ATP. The release caused by UTP was virtually una ected by RB-2. However, these P2-agonists failed to elicit a contraction of the segment. 5 The potency order of all the agonists tested for the release of ATP was a,b-mATP4UTP4b,gmATP4ADP.6 In superfusion experiments with cultured smooth muscle cells from the ileum, a,b-mATP (100 mM) enhanced the release of ATP 5 fold above the basal value. This evoked release was inhibited by RB-2. 7 These ®ndings suggest that ATP release and contraction induced by P2-agonists such as a,b-mATP in the guinea-pig ileum result mainly from stimulation of di erent P2-purinoceptors, P2Y-like purinoceptors on the smooth muscles and, probably, P2X-purinoceptors on cholinergic nerve terminals, respectively. However, the ATP release may also be mediated, in part, by P2U-receptors, because UTP caused RB-2-insensitive ATP release.

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Postjunctional ATP release mediated by stimulation of P2x-purinoceptors

Cited by 2 publications

References 1 publication

Degranulation of human mast cells: modulation by P2 receptors’ agonists

Degranulation of human mast cells: modulation by P2 receptors’ agonists

ATP release and contraction mediated by different P2‐receptor subtypes in guinea‐pig ileal smooth muscle

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