Pannexin 1 facilitates arterial relaxation via an endothelium-derived hyperpolarization mechanism

Dina Gaynullina; Valery I. Shestopalov; Yury Panchin; Olga S. Tarasova

doi:10.1016/j.febslet.2015.03.018

Pannexin 1 facilitates arterial relaxation via an endothelium-derived hyperpolarization mechanism

Dina Gaynullina, Valery I. Shestopalov, Yury Panchin, Olga S. Tarasova

Ophthalmology

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

Pannexin 1 (Panx1) is involved in endothelium-dependent vasodilation in large arteries, but the exact mechanistic role remains poorly understood. We hypothesized that Panx1 facilitates large vessel relaxations regulating endothelium-derived hyperpolarization (EDH)-like mechanisms. The EDH-like component of acetylcholine-induced relaxation of saphenous arteries studied in isometric myograph after inhibition of NO-synthase and cyclooxygenase was significantly impaired in mice with genetically ablated Panx1 (KO) relative to that in the wild type (WT) mice. Application of P1-receptor antagonist and apyrase significantly reduced this component in WT, but not in KO mice, indicating participation of ATP released via Panx1 in the EDH-like relaxation.

Original language	English (US)
Pages (from-to)	1164-1170
Number of pages	7
Journal	FEBS letters
Volume	589
Issue number	10
DOIs	https://doi.org/10.1016/j.febslet.2015.03.018
State	Published - Apr 28 2015

Keywords

ATP
EDHF
Endothelium
Endothelium-derived hyperpolarization
Knockout mice
Pannexin 1
Pannexins
Saphenous artery

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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title = "Pannexin 1 facilitates arterial relaxation via an endothelium-derived hyperpolarization mechanism",

abstract = "Pannexin 1 (Panx1) is involved in endothelium-dependent vasodilation in large arteries, but the exact mechanistic role remains poorly understood. We hypothesized that Panx1 facilitates large vessel relaxations regulating endothelium-derived hyperpolarization (EDH)-like mechanisms. The EDH-like component of acetylcholine-induced relaxation of saphenous arteries studied in isometric myograph after inhibition of NO-synthase and cyclooxygenase was significantly impaired in mice with genetically ablated Panx1 (KO) relative to that in the wild type (WT) mice. Application of P1-receptor antagonist and apyrase significantly reduced this component in WT, but not in KO mice, indicating participation of ATP released via Panx1 in the EDH-like relaxation.",

keywords = "ATP, EDHF, Endothelium, Endothelium-derived hyperpolarization, Knockout mice, Pannexin 1, Pannexins, Saphenous artery",

author = "Dina Gaynullina and Shestopalov, {Valery I.} and Yury Panchin and Tarasova, {Olga S.}",

note = "Funding Information: The authors thank Dr. Alexander Gaydukov for providing ouabain; Dr. Laird, S. Penuela and G. Sosinsky for kind gifts of Panx1 antibodies; Dr. G. Dvoriantchikova for the help with artery dissection and preparation. This work was supported by the Russian Science Foundation (Grant number 14-15-00704 ). Publisher Copyright: {\textcopyright} 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.",

year = "2015",

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doi = "10.1016/j.febslet.2015.03.018",

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AU - Gaynullina, Dina

AU - Shestopalov, Valery I.

AU - Panchin, Yury

AU - Tarasova, Olga S.

N1 - Funding Information: The authors thank Dr. Alexander Gaydukov for providing ouabain; Dr. Laird, S. Penuela and G. Sosinsky for kind gifts of Panx1 antibodies; Dr. G. Dvoriantchikova for the help with artery dissection and preparation. This work was supported by the Russian Science Foundation (Grant number 14-15-00704 ). Publisher Copyright: © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

PY - 2015/4/28

Y1 - 2015/4/28

N2 - Pannexin 1 (Panx1) is involved in endothelium-dependent vasodilation in large arteries, but the exact mechanistic role remains poorly understood. We hypothesized that Panx1 facilitates large vessel relaxations regulating endothelium-derived hyperpolarization (EDH)-like mechanisms. The EDH-like component of acetylcholine-induced relaxation of saphenous arteries studied in isometric myograph after inhibition of NO-synthase and cyclooxygenase was significantly impaired in mice with genetically ablated Panx1 (KO) relative to that in the wild type (WT) mice. Application of P1-receptor antagonist and apyrase significantly reduced this component in WT, but not in KO mice, indicating participation of ATP released via Panx1 in the EDH-like relaxation.

AB - Pannexin 1 (Panx1) is involved in endothelium-dependent vasodilation in large arteries, but the exact mechanistic role remains poorly understood. We hypothesized that Panx1 facilitates large vessel relaxations regulating endothelium-derived hyperpolarization (EDH)-like mechanisms. The EDH-like component of acetylcholine-induced relaxation of saphenous arteries studied in isometric myograph after inhibition of NO-synthase and cyclooxygenase was significantly impaired in mice with genetically ablated Panx1 (KO) relative to that in the wild type (WT) mice. Application of P1-receptor antagonist and apyrase significantly reduced this component in WT, but not in KO mice, indicating participation of ATP released via Panx1 in the EDH-like relaxation.

KW - ATP

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KW - Endothelium

KW - Endothelium-derived hyperpolarization

KW - Knockout mice

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KW - Saphenous artery

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Pannexin 1 facilitates arterial relaxation via an endothelium-derived hyperpolarization mechanism

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