scholarly journals P2X4 Receptors Mediate Ca2+ Release from Lysosomes in Response to Stimulation of P2X7 and H1 Histamine Receptors

2021 ◽  
Vol 22 (19) ◽  
pp. 10492
Author(s):  
Sin-Lih Tan ◽  
Muruj Barri ◽  
Peace Atakpa-Adaji ◽  
Colin W. Taylor ◽  
Ewan St. John Smith ◽  
...  
Keyword(s):  
Membrane Trafficking ◽  
P2x7 Receptor ◽  
Purinergic Receptor ◽  
Histamine Receptor ◽  
Receptor Activation ◽  
Receptor Stimulation ◽  
Inward Current ◽  
P2x4 Receptors ◽  
P2x7 Receptor Activation ◽  
Stimulation Of

The P2X4 purinergic receptor is targeted to endolysosomes, where it mediates an inward current dependent on luminal ATP and pH. Activation of P2X4 receptors was previously shown to trigger lysosome fusion, but the regulation of P2X4 receptors and their role in lysosomal Ca2+ signaling are poorly understood. We show that lysosomal P2X4 receptors are activated downstream of plasma membrane P2X7 and H1 histamine receptor stimulation. When P2X4 receptors are expressed, the increase in near-lysosome cytosolic [Ca2+] is exaggerated, as detected with a low-affinity targeted Ca2+ sensor. P2X4-dependent changes in lysosome properties were triggered downstream of P2X7 receptor activation, including an enlargement of lysosomes indicative of homotypic fusion and a redistribution of lysosomes towards the periphery of the cell. Lysosomal P2X4 receptors, therefore, have a role in regulating lysosomal Ca2+ release and the regulation of lysosomal membrane trafficking.

scholarly journals Possible Involvement of P2X7 Receptor Activation in Microglial Neuroprotection against Focal Cerebral Ischemia in Rats

2008 ◽  
Vol 31 (6) ◽  
pp. 1121-1130 ◽  
Author(s):  
Daijiro Yanagisawa ◽  
Yoshihisa Kitamura ◽  
Kazuyuki Takata ◽  
Izumi Hide ◽  
Yoshihiro Nakata ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
P2x7 Receptor ◽  
Focal Cerebral Ischemia ◽  
Receptor Activation ◽  
P2x7 Receptor Activation

Calmidazolium selectively inhibits exocytotic glutamate release evoked by P2X7 receptor activation

2012 ◽  
Vol 60 (8) ◽  
pp. 768-772 ◽  
Author(s):  
Chiara Cervetto ◽  
Maria Chiara Mazzotta ◽  
Daniela Frattaroli ◽  
Susanna Alloisio ◽  
Mario Nobile ◽  
...  
Keyword(s):  
P2x7 Receptor ◽  
Glutamate Release ◽  
Receptor Activation ◽  
P2x7 Receptor Activation

ANG II AT2 receptor modulates AT1receptor-mediated descending vasa recta endothelial Ca2+ signaling

2003 ◽  
Vol 284 (3) ◽  
pp. H779-H789 ◽  
Author(s):  
Kristie Rhinehart ◽  
Corey A. Handelsman ◽  
Erik P. Silldorff ◽  
Thomas L. Pallone
Keyword(s):  
Receptor Agonist ◽  
Calcium Concentration ◽  
Cyclopiazonic Acid ◽  
Receptor Activation ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Receptor Stimulation ◽  
Vasa Recta ◽  
Stimulation Of

We tested whether the respective angiotensin type 1 (AT1) and 2 (AT2) receptor subtype antagonists losartan and PD-123319 could block the descending vasa recta (DVR) endothelial intracellular calcium concentration ([Ca2+]i) suppression induced by ANG II. ANG II partially reversed the increase in [Ca2+]igenerated by cyclopiazonic acid (CPA; 10−5 M), acetylcholine (ACh; 10−5 M), or bradykinin (BK; 10−7 M). Losartan (10−5 M) blocked that effect. When vessels were treated with ANG II before stimulation with BK and ACh, concomitant AT2 receptor blockade with PD-123319 (10−8 M) augmented the suppression of endothelial [Ca2+]i responses. Similarly, preactivation with the AT2 receptor agonist CGP-42112A (10−8 M) prevented AT1 receptor stimulation with ANG II + PD-123319 from suppressing endothelial [Ca2+]i. In contrast to endothelial [Ca2+]i suppression by ANG II, pericyte [Ca2+]i exhibited typical peak and plateau [Ca2+]i responses that were blocked by losartan but not PD-123319. DVR vasoconstriction by ANG II was augmented when AT2 receptors were blocked with PD-123319. Similarly, AT2 receptor stimulation with CGP-42112A delayed the onset of ANG II-induced constriction. PD-123319 alone (10−5 M) showed no AT1-like action to constrict microperfused DVR or increase pericyte [Ca2+]i. We conclude that ANG II suppression of endothelial [Ca2+]i and stimulation of pericyte [Ca2+]i is mediated by AT1 or AT1-like receptors. Furthermore, AT2 receptor activation opposes ANG II-induced endothelial [Ca2+]i suppression and abrogates ANG II-induced DVR vasoconstriction.

MSU Crystals induce sterile IL-1β secretion via P2X7 receptor activation and HMGB1 release

2020 ◽  
Vol 1864 (1) ◽  
pp. 129461 ◽  
Author(s):  
Ygor Marinho ◽  
Camila Marques-da-Silva ◽  
Patricia Teixeira Santana ◽  
Mariana Martins Chaves ◽  
Augusto Shuiti Tamura ◽  
...  
Keyword(s):  
P2x7 Receptor ◽  
Receptor Activation ◽  
P2x7 Receptor Activation ◽  
Msu Crystals

scholarly journals P2X7 receptor activation regulates rapid unconventional export of transglutaminase-2

2015 ◽  
Vol 128 (24) ◽  
pp. 4615-4628 ◽  
Author(s):  
M. Adamczyk ◽  
R. Griffiths ◽  
S. Dewitt ◽  
V. Kna uper ◽  
D. Aeschlimann
Keyword(s):  
P2x7 Receptor ◽  
Transglutaminase 2 ◽  
Receptor Activation ◽  
P2x7 Receptor Activation

scholarly journals P2X7 receptor activation regulates microglial cell death during oxygen-glucose deprivation

2013 ◽  
Vol 73 ◽  
pp. 311-319 ◽  
Author(s):  
Ukpong B. Eyo ◽  
Sam A. Miner ◽  
Katelin E. Ahlers ◽  
Long-Jun Wu ◽  
Michael E. Dailey
Keyword(s):  
Cell Death ◽  
P2x7 Receptor ◽  
Microglial Cell ◽  
Glucose Deprivation ◽  
Receptor Activation ◽  
Oxygen Glucose Deprivation ◽  
P2x7 Receptor Activation

scholarly journals P2X7 receptor activation induces cell death and microparticle release in murine erythroleukemia cells

2010 ◽  
Vol 1798 (9) ◽  
pp. 1797-1804 ◽  
Author(s):  
Patrick Constantinescu ◽  
Bin Wang ◽  
Kati Kovacevic ◽  
Iman Jalilian ◽  
Giel J.C.G.M. Bosman ◽  
...  
Keyword(s):  
Cell Death ◽  
P2x7 Receptor ◽  
Receptor Activation ◽  
Erythroleukemia Cells ◽  
Murine Erythroleukemia ◽  
P2x7 Receptor Activation ◽  
Murine Erythroleukemia Cells

The stimulation of inositol lipid metabolism that accompanies calcium mobilization in stimulated cells: defined characteristics and unanswered questions

1981 ◽  
Vol 296 (1080) ◽  
pp. 123-138 ◽  
Keyword(s):  
Calcium Concentration ◽  
Receptor Activation ◽  
Receptor Stimulation ◽  
Stimulus Response ◽  
Inositol Lipids ◽  
Inositol Phospholipid ◽  
Inositol Phospholipid Breakdown ◽  
Phosphatidylinositol 4 ◽  
Hydrolysis Of ◽  
Stimulation Of

It now appears to be generally agreed that the ‘phosphatidylinositol response’, discovered in 1953 by Hokin & Hokin, occurs universally when cells are stimulated by ligands that cause an elevation of the ionized calcium concentration of the cytosol. The initiating reaction is almost certainly hydrolysis of an inositol lipid by a phosphodiesterase. Phosphatidylinositol, phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate all break down rapidly under such circumstances. However, we do not yet know which of these individual reactions is most closely coupled to receptor stimulation, nor do we know where in the cell it occurs. With many stimuli, inositol phospholipid breakdown is closely coupled to occupation of receptors and appears not to be a response to changes in cytosol [Ca 2+ ] : this provoked the suggestion that it may be a reaction essential to the coupling between activation of receptors and the mobilization of Ca 2+ within the cell. In a few situations, however, it appears probable that inositol lipid breakdown can occur as a result of the rise in cytosol [Ca 2+ ] that follows receptor activation: such observations gave rise to the alternative opinion that inositol lipid breakdown cannot be related to stimulus-response coupling at calcium-mobilizing receptors. It now seems likely that these two views are too rigidly polarized and that some cells probably display both receptor-linked and Ca 2+ -controlled breakdown of inositol lipids. Both may sometimes occur simultaneously or sequentially in the same cell.

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