Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo
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 triggere...
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| Vydané v: | Cell Ročník 139; číslo 6; s. 1143 |
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| Hlavní autori: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
11.12.2009
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| Predmet: | |
| ISSN: | 1097-4172, 1097-4172 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| 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. |
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| AbstractList | 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.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. 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. |
| Author | Schmidbauer, Stefan Spronk, Henri M Morrissey, James H Renné, Thomas Mutch, Nicola J Gahl, William A Esterl, Lucie Müller, Felicitas Schenk, Wolfdieter A Smith, Stephanie A |
| Author_xml | – sequence: 1 givenname: Felicitas surname: Müller fullname: Müller, Felicitas organization: Department of Molecular Medicine and Surgery and Center for Molecular Medicine, Karolinska Institutet, Stockholm S-171 76, Sweden – sequence: 2 givenname: Nicola J surname: Mutch fullname: Mutch, Nicola J – sequence: 3 givenname: Wolfdieter A surname: Schenk fullname: Schenk, Wolfdieter A – sequence: 4 givenname: Stephanie A surname: Smith fullname: Smith, Stephanie A – sequence: 5 givenname: Lucie surname: Esterl fullname: Esterl, Lucie – sequence: 6 givenname: Henri M surname: Spronk fullname: Spronk, Henri M – sequence: 7 givenname: Stefan surname: Schmidbauer fullname: Schmidbauer, Stefan – sequence: 8 givenname: William A surname: Gahl fullname: Gahl, William A – sequence: 9 givenname: James H surname: Morrissey fullname: Morrissey, James H – sequence: 10 givenname: Thomas surname: Renné fullname: Renné, Thomas |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20005807$$D View this record in MEDLINE/PubMed |
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| References | 21082980 - Expert Rev Hematol. 2010 Jun;3(3):269-72. doi: 10.1586/ehm.10.26. |
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| Title | Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo |
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