Decavanadate, a P2X receptor antagonist, and its use to study ligand interactions with P2X7 receptors

Michel, Anton D.; Xing, M; Thompson, K M; Jones, Clare A.; Humphrey, P. P. A.

doi:10.1016/j.ejphar.2006.01.009

Cited by 40 publications

(45 citation statements)

References 31 publications

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“…In membranes, decavanadate has been found to modulate transient receptor protein channels [53] and also to be a nucleotide P2X receptor antagonist [124]. It is therefore useful as a tool in the study of specific ligand interactions with these proteins.…”

Section: Decavanadate Interactions and Effects In Proteinsmentioning

confidence: 99%

Decavanadate (V10O286-) and oxovanadates: Oxometalates with many biological activities

Aureliano

Crans

2009

Journal of Inorganic Biochemistry

227

250

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Section: Decavanadate Interactions and Effects In Proteinsmentioning

confidence: 99%

Decavanadate (V10O286-) and oxovanadates: Oxometalates with many biological activities

Aureliano

Crans

2009

Journal of Inorganic Biochemistry

227

250

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“…14,21 Wound sizes were measured 12 hours after injury. Treatment with oxATP resulted in a significantly larger wound area (Figure 2A), supporting previous findings that P2X7 promotes wound healing.…”

Section: Effects Of P2x7 Inhibition On Corneal Epithelial Wound Closurementioning

confidence: 99%

Purinoreceptor P2X7 Regulation of Ca2+ Mobilization and Cytoskeletal Rearrangement Is Required for Corneal Reepithelialization after Injury

Minns

Teicher

Rich

et al. 2016

The American Journal of Pathology

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The process of wound healing involves a complex network of signaling pathways working to promote rapid cell migration and wound closure. Activation of purinergic receptors by secreted nucleotides plays a major role in calcium mobilization and the subsequent calcium-dependent signaling that is essential for proper healing. The role of the purinergic receptor P2X7 in wound healing is still relatively unknown. We demonstrate that P2X7 expression increases at the leading edge of corneal epithelium after injury in an organ culture model, and that this change occurs despite an overall decrease in P2X7 expression throughout the epithelium. Inhibition of P2X7 prevents this change in localization after injury and impairs wound healing. In cell culture, P2X7 inhibition attenuates the amplitude and duration of injuryinduced calcium mobilization in cells at the leading edge. Immunofluorescence analysis of scratchwounded cells reveals that P2X7 inhibition results in an overall decrease in the number of focal adhesions along with a concentration of focal adhesions at the wound margin. Live cell imaging of green fluorescent proteinelabeled actin and talin shows that P2X7 inhibition alters actin cytoskeletal rearrangements and focal adhesion dynamics after injury. Together, these data demonstrate that P2X7 plays a critical role in mediating calcium signaling and coordinating cytoskeletal rearrangement at the leading edge, both of which processes are early signaling events necessary for proper epithelial wound healing. (Am J Pathol 2016, 186: 285e296; http://dx

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“…Decavanadate [26] and the pyrazole derivative N-[4-3,5-bis(trifluromethyl)pyrazol-1-yl]-4-methyl-1,2,3-thiadiazole-5-carboxamide (BTP2) [27] potentiate Ca 2+ -dependent TRPM4 activity, but these agents lack specificity. Decavanadate has effects on inositol 1,4,5 trisphosphate (IP 3 ) receptors and purinoreceptors (P2X) [28] whereas BTP2 inhibits TRPC3 and TRPC5 channels [29]. Flufenamic acid and clotrimazole act as gating inhibitors, and spermine and Gd 3+ as pore blockers [19, 30–32] but these agents are not selective for TRPM4 and influence many other channels.…”

Section: Trpm4 Pharmacologymentioning

confidence: 99%

TRPM4 channels in smooth muscle function

Earley

2013

Pflugers Arch - Eur J Physiol

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The melastatin (M) Transient Receptor Potential (TRP) channel TRPM4 is selective for monovalent cations and is activated by high levels of intracellular Ca2+. TRPM4 is broadly distributed and may be involved in numerous functions, including electrical conduction in the heart, respiratory rhythm, immune response, and secretion of insulin by pancreatic β cells. The significance of TRPM4 in smooth muscle cell function is reviewed here. Several studies indicate that TRPM4 channels are critically important for pressure-induced cerebral arterial myocyte depolarization and myogenic vasoconstriction as well as autoregulation of cerebral blood flow. Regulation of TRPM4 activity in arterial smooth muscle cells is complex, and involves release of Ca2+ from the sarcoplasmic reticulum through inositol 1,4,5 trisphosphate receptors and translocation of TRPM4 channels to the plasma membrane in response to Protein Kinase Cδ. TRPM4 is also present in colonic, urinary bladder, aortic, interlobar pulmonary and renal artery, airway, and corpus cavernosum smooth muscle cells, but its significance and regulation in these tissues is less well-characterized.

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Decavanadate, a P2X receptor antagonist, and its use to study ligand interactions with P2X7 receptors

Cited by 40 publications

References 31 publications

Decavanadate (V10O286-) and oxovanadates: Oxometalates with many biological activities

Decavanadate (V10O286-) and oxovanadates: Oxometalates with many biological activities

Purinoreceptor P2X7 Regulation of Ca2+ Mobilization and Cytoskeletal Rearrangement Is Required for Corneal Reepithelialization after Injury

TRPM4 channels in smooth muscle function

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