The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.

Research output: Contribution to conferencePosterResearchpeer-review

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The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction. / Bouzinova, Elena.

2015. Poster session presented at Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark.

Research output: Contribution to conferencePosterResearchpeer-review

Harvard

Bouzinova, E 2015, 'The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.', Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark, 17/09/2015 - 20/09/2015.

APA

Bouzinova, E. (2015). The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.. Poster session presented at Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark.

CBE

Bouzinova E. 2015. The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction. Poster session presented at Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark.

MLA

Bouzinova, Elena The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.. Scandinavian Physiological Society Annual Meeting, 17 Sep 2015, Aarhus, Denmark, Poster, 2015. 1 p.

Vancouver

Bouzinova E. The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.. 2015. Poster session presented at Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark.

Author

Bouzinova, Elena. / The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction. Poster session presented at Scandinavian Physiological Society Annual Meeting, Aarhus, Denmark.1 p.

Bibtex

@conference{98b3ca76e30346ebbcb4e5b6dd65acbb,
title = "The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.",
abstract = "Aim: Na,K-ATPase is essential for maintaining the transmembrane ion gradient and might initiate various intracellular signaling. These signals possibly act through a modification of the local ion concentrations or via Src-kinase activation. It is known that inhibition of the α-2 isoform of Na,K-ATPase by ouabain elevates blood pressure. Consequently, ouabain was shown to potentiate arterial contraction in vitro. In contrast, we have demonstrated that siRNA-induced down-regulation of the α-2 isoform Na,K-ATPase expression reduced arterial sensitivity to agonist stimulation and prevented the effect of ouabain. Here we demonstrate results of our research on the mechanisms involved in the modulation of vascular wall contractility by ouabain-sensitive Na,K-ATPase. Methods: The experiments were performed using rat mesenteric arteries in isometric myograph conditions. To inhibit kinase activity a Src-family selective tyrosine kinase inhibitor, PP2, and pNaKtide - a membrane-permeable small peptide which antagonizes ouabain-induced activation of Src-kinase were used. Results: The pro-contractile action of ouabain is associated with activation of Src. This is supported by Western blot analyses showing activation of Src by ouabain and its inhibition by pNaKtide. Src was also activated by agonist (noradrenaline - NA) stimulation. Src-dependent potentiation of vasoconstriction was associated with sensitization of contractile machinery to [Ca2+]i, as evident from MYPT (myosin phosphatase targeting protein) phosphorylation assay. Down-regulation of the α-2 isoform Na,K-ATPase prevented the inhibitory effect of Src inhibitors on arterial contraction. Conclusions: The pro-contractile action of ouabain-sensitive Na,K-ATPase inhibition is associated with Src-kinase inhibition suggesting the role of this signaling pathway in regulation of vascular tone and peripheral resistance.",
keywords = "NA+/K+-ATPASE, pNaKtide, Vascular wall",
author = "Elena Bouzinova",
year = "2015",
month = "9",
day = "18",
language = "English",
note = "Scandinavian Physiological Society Annual Meeting, SPS 2015 ; Conference date: 17-09-2015 Through 20-09-2015",

}

RIS

TY - CONF

T1 - The role of Na,K-ATPase/Src-kinase signaling pathway in the vascular wall contaction.

AU - Bouzinova, Elena

PY - 2015/9/18

Y1 - 2015/9/18

N2 - Aim: Na,K-ATPase is essential for maintaining the transmembrane ion gradient and might initiate various intracellular signaling. These signals possibly act through a modification of the local ion concentrations or via Src-kinase activation. It is known that inhibition of the α-2 isoform of Na,K-ATPase by ouabain elevates blood pressure. Consequently, ouabain was shown to potentiate arterial contraction in vitro. In contrast, we have demonstrated that siRNA-induced down-regulation of the α-2 isoform Na,K-ATPase expression reduced arterial sensitivity to agonist stimulation and prevented the effect of ouabain. Here we demonstrate results of our research on the mechanisms involved in the modulation of vascular wall contractility by ouabain-sensitive Na,K-ATPase. Methods: The experiments were performed using rat mesenteric arteries in isometric myograph conditions. To inhibit kinase activity a Src-family selective tyrosine kinase inhibitor, PP2, and pNaKtide - a membrane-permeable small peptide which antagonizes ouabain-induced activation of Src-kinase were used. Results: The pro-contractile action of ouabain is associated with activation of Src. This is supported by Western blot analyses showing activation of Src by ouabain and its inhibition by pNaKtide. Src was also activated by agonist (noradrenaline - NA) stimulation. Src-dependent potentiation of vasoconstriction was associated with sensitization of contractile machinery to [Ca2+]i, as evident from MYPT (myosin phosphatase targeting protein) phosphorylation assay. Down-regulation of the α-2 isoform Na,K-ATPase prevented the inhibitory effect of Src inhibitors on arterial contraction. Conclusions: The pro-contractile action of ouabain-sensitive Na,K-ATPase inhibition is associated with Src-kinase inhibition suggesting the role of this signaling pathway in regulation of vascular tone and peripheral resistance.

AB - Aim: Na,K-ATPase is essential for maintaining the transmembrane ion gradient and might initiate various intracellular signaling. These signals possibly act through a modification of the local ion concentrations or via Src-kinase activation. It is known that inhibition of the α-2 isoform of Na,K-ATPase by ouabain elevates blood pressure. Consequently, ouabain was shown to potentiate arterial contraction in vitro. In contrast, we have demonstrated that siRNA-induced down-regulation of the α-2 isoform Na,K-ATPase expression reduced arterial sensitivity to agonist stimulation and prevented the effect of ouabain. Here we demonstrate results of our research on the mechanisms involved in the modulation of vascular wall contractility by ouabain-sensitive Na,K-ATPase. Methods: The experiments were performed using rat mesenteric arteries in isometric myograph conditions. To inhibit kinase activity a Src-family selective tyrosine kinase inhibitor, PP2, and pNaKtide - a membrane-permeable small peptide which antagonizes ouabain-induced activation of Src-kinase were used. Results: The pro-contractile action of ouabain is associated with activation of Src. This is supported by Western blot analyses showing activation of Src by ouabain and its inhibition by pNaKtide. Src was also activated by agonist (noradrenaline - NA) stimulation. Src-dependent potentiation of vasoconstriction was associated with sensitization of contractile machinery to [Ca2+]i, as evident from MYPT (myosin phosphatase targeting protein) phosphorylation assay. Down-regulation of the α-2 isoform Na,K-ATPase prevented the inhibitory effect of Src inhibitors on arterial contraction. Conclusions: The pro-contractile action of ouabain-sensitive Na,K-ATPase inhibition is associated with Src-kinase inhibition suggesting the role of this signaling pathway in regulation of vascular tone and peripheral resistance.

KW - NA+/K+-ATPASE

KW - pNaKtide

KW - Vascular wall

M3 - Poster

ER -