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Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo

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Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo. / Müller, Felicitas; Mutch, Nicola J; Schenk, Wolfdieter A; Smith, Stephanie A; Esterl, Lucie; Spronk, Henri M; Schmidbauer, Stefan; Gahl, William A; Morrissey, James H; Renné, Thomas.

in: CELL, Jahrgang 139, Nr. 6, 11.12.2009, S. 1143-56.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Müller, F, Mutch, NJ, Schenk, WA, Smith, SA, Esterl, L, Spronk, HM, Schmidbauer, S, Gahl, WA, Morrissey, JH & Renné, T 2009, 'Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo', CELL, Jg. 139, Nr. 6, S. 1143-56. https://doi.org/10.1016/j.cell.2009.11.001

APA

Müller, F., Mutch, N. J., Schenk, W. A., Smith, S. A., Esterl, L., Spronk, H. M., Schmidbauer, S., Gahl, W. A., Morrissey, J. H., & Renné, T. (2009). Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo. CELL, 139(6), 1143-56. https://doi.org/10.1016/j.cell.2009.11.001

Vancouver

Müller F, Mutch NJ, Schenk WA, Smith SA, Esterl L, Spronk HM et al. Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo. CELL. 2009 Dez 11;139(6):1143-56. https://doi.org/10.1016/j.cell.2009.11.001

Bibtex

@article{98860d42e67746cb82173349e64734c0,
title = "Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo",
abstract = "Platelets play a central role in thrombosis, hemostasis, and inflammation. We show that activated platelets release inorganic polyphosphate (polyP), a polymer of 60-100 phosphate residues that directly bound to and activated the plasma protease factor XII. PolyP-driven factor XII activation triggered release of the inflammatory mediator bradykinin by plasma kallikrein-mediated kininogen processing. PolyP increased vascular permeability and induced fluid extravasation in skin microvessels of mice. Mice deficient in factor XII or bradykinin receptors were resistant to polyP-induced leakage. PolyP initiated clotting of plasma via the contact pathway. Ablation of intrinsic coagulation pathway proteases factor XII and factor XI protected mice from polyP-triggered lethal pulmonary embolism. Targeting polyP with phosphatases interfered with procoagulant activity of activated platelets and blocked platelet-induced thrombosis in mice. Addition of polyP restored defective plasma clotting of Hermansky-Pudlak Syndrome patients, who lack platelet polyP. The data identify polyP as a new class of mediator having fundamental roles in platelet-driven proinflammatory and procoagulant disorders.",
keywords = "Animals, Blood Platelets, Bradykinin, Factor XII, Fibrin, Hermanski-Pudlak Syndrome, Humans, Inflammation Mediators, Mice, Peptide Hydrolases, Plasma, Polyphosphates, Receptors, Bradykinin, Thrombosis",
author = "Felicitas M{\"u}ller and Mutch, {Nicola J} and Schenk, {Wolfdieter A} and Smith, {Stephanie A} and Lucie Esterl and Spronk, {Henri M} and Stefan Schmidbauer and Gahl, {William A} and Morrissey, {James H} and Thomas Renn{\'e}",
year = "2009",
month = dec,
day = "11",
doi = "10.1016/j.cell.2009.11.001",
language = "English",
volume = "139",
pages = "1143--56",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo

AU - Müller, Felicitas

AU - Mutch, Nicola J

AU - Schenk, Wolfdieter A

AU - Smith, Stephanie A

AU - Esterl, Lucie

AU - Spronk, Henri M

AU - Schmidbauer, Stefan

AU - Gahl, William A

AU - Morrissey, James H

AU - Renné, Thomas

PY - 2009/12/11

Y1 - 2009/12/11

N2 - Platelets play a central role in thrombosis, hemostasis, and inflammation. We show that activated platelets release inorganic polyphosphate (polyP), a polymer of 60-100 phosphate residues that directly bound to and activated the plasma protease factor XII. PolyP-driven factor XII activation triggered release of the inflammatory mediator bradykinin by plasma kallikrein-mediated kininogen processing. PolyP increased vascular permeability and induced fluid extravasation in skin microvessels of mice. Mice deficient in factor XII or bradykinin receptors were resistant to polyP-induced leakage. PolyP initiated clotting of plasma via the contact pathway. Ablation of intrinsic coagulation pathway proteases factor XII and factor XI protected mice from polyP-triggered lethal pulmonary embolism. Targeting polyP with phosphatases interfered with procoagulant activity of activated platelets and blocked platelet-induced thrombosis in mice. Addition of polyP restored defective plasma clotting of Hermansky-Pudlak Syndrome patients, who lack platelet polyP. The data identify polyP as a new class of mediator having fundamental roles in platelet-driven proinflammatory and procoagulant disorders.

AB - Platelets play a central role in thrombosis, hemostasis, and inflammation. We show that activated platelets release inorganic polyphosphate (polyP), a polymer of 60-100 phosphate residues that directly bound to and activated the plasma protease factor XII. PolyP-driven factor XII activation triggered release of the inflammatory mediator bradykinin by plasma kallikrein-mediated kininogen processing. PolyP increased vascular permeability and induced fluid extravasation in skin microvessels of mice. Mice deficient in factor XII or bradykinin receptors were resistant to polyP-induced leakage. PolyP initiated clotting of plasma via the contact pathway. Ablation of intrinsic coagulation pathway proteases factor XII and factor XI protected mice from polyP-triggered lethal pulmonary embolism. Targeting polyP with phosphatases interfered with procoagulant activity of activated platelets and blocked platelet-induced thrombosis in mice. Addition of polyP restored defective plasma clotting of Hermansky-Pudlak Syndrome patients, who lack platelet polyP. The data identify polyP as a new class of mediator having fundamental roles in platelet-driven proinflammatory and procoagulant disorders.

KW - Animals

KW - Blood Platelets

KW - Bradykinin

KW - Factor XII

KW - Fibrin

KW - Hermanski-Pudlak Syndrome

KW - Humans

KW - Inflammation Mediators

KW - Mice

KW - Peptide Hydrolases

KW - Plasma

KW - Polyphosphates

KW - Receptors, Bradykinin

KW - Thrombosis

U2 - 10.1016/j.cell.2009.11.001

DO - 10.1016/j.cell.2009.11.001

M3 - SCORING: Journal article

C2 - 20005807

VL - 139

SP - 1143

EP - 1156

JO - CELL

JF - CELL

SN - 0092-8674

IS - 6

ER -