loading...| Preferred Name | Platelet homeostasis | |
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Authored: Akkerman, JW, 2009-06-03 Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). Cyclooxygenase-2 (COX-2) and endothelial nitric oxide synthase (eNOS) are primarily expressed in endothelial cells. Both are important regulators of vascular function. Under normal conditions, laminar flow induces vascular endothelial COX-2 expression and synthesis of Prostacyclin (PGI2) which in turn stimulates endothelial Nitric Oxide Synthase (eNOS) activity. PGI2 and NO both oppose platelet activation and aggregation, as does the CD39 ecto-ADPase, which decreases platelet activation and recruitment by metabolizing platelet-released ADP. Edited: Jupe, S, 2010-06-07 Reviewed: Kunapuli, SP, 2010-06-07 |
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http://purl.obolibrary.org/obo/HINO_0015219 |
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Authored: Akkerman, JW, 2009-06-03 Under normal conditions the vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma, vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and by the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction (Becker et al. 2000). Cyclooxygenase-2 (COX-2) and endothelial nitric oxide synthase (eNOS) are primarily expressed in endothelial cells. Both are important regulators of vascular function. Under normal conditions, laminar flow induces vascular endothelial COX-2 expression and synthesis of Prostacyclin (PGI2) which in turn stimulates endothelial Nitric Oxide Synthase (eNOS) activity. PGI2 and NO both oppose platelet activation and aggregation, as does the CD39 ecto-ADPase, which decreases platelet activation and recruitment by metabolizing platelet-released ADP. Edited: Jupe, S, 2010-06-07 Reviewed: Kunapuli, SP, 2010-06-07 |
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| definition source |
Reactome, http://www.reactome.org Pubmed10798271 Pubmed16297879 |
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Platelet homeostasis |
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HINO:0015219 |
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Platelet homeostasis |
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| seeAlso |
Reactome Database ID Release 43418346 ReactomeREACT_23876 |
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http://purl.obolibrary.org/obo/HINO_0015220 http://purl.obolibrary.org/obo/HINO_0014542 http://purl.obolibrary.org/obo/HINO_0015213 |