CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates
OBJECTIVE—Soluble CD40 ligand (sCD40L) has been recently implicated in the pathogenesis of atherosclerosis. Elevated levels of sCD40L in acute coronary syndrome patients suggests enhanced platelet function; however, the exact mechanism by which this occurs is unknown. In this study, we examined the...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2428-2434 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Chakrabarti, Subrata Varghese, Sonia Vitseva, Olga Tanriverdi, Kahraman Freedman, Jane E |
| description | OBJECTIVE—Soluble CD40 ligand (sCD40L) has been recently implicated in the pathogenesis of atherosclerosis. Elevated levels of sCD40L in acute coronary syndrome patients suggests enhanced platelet function; however, the exact mechanism by which this occurs is unknown. In this study, we examined the effect of sCD40L on platelet function and reactive oxygen and nitrogen species (RONS) generation.
METHODS AND RESULTS—Platelet stimulation in the presence of recombinant sCD40L (rsCD40L) led to enhanced generation of RONS as measured by DCFHDA oxidation and confocal microscopy. Incubation with rsCD40L led to enhanced platelet P-selectin expression, aggregation, and platelet-leukocyte conjugation. Platelets isolated from CD40L-deficient mice had decreased agonist-induced NO release as compared with wild-type mice. Incubation of platelets with rsCD40L enhanced stimulation-induced p38 MAP kinase and Akt phosphorylation.
CONCLUSION—Soluble CD40L enhances platelet activation, aggregation, and platelet-leukocyte conjugation, as well as increases stimulation-induced platelet release of RONS through activation of Akt and p38 MAP kinase signaling pathways. These data suggest that sCD40L regulates platelet-dependent inflammatory and thrombotic responses that contribute to the pathogenesis of atherothrombosis. |
| doi_str_mv | 10.1161/01.ATV.0000184765.59207.f3 |
| format | Article |
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METHODS AND RESULTS—Platelet stimulation in the presence of recombinant sCD40L (rsCD40L) led to enhanced generation of RONS as measured by DCFHDA oxidation and confocal microscopy. Incubation with rsCD40L led to enhanced platelet P-selectin expression, aggregation, and platelet-leukocyte conjugation. Platelets isolated from CD40L-deficient mice had decreased agonist-induced NO release as compared with wild-type mice. Incubation of platelets with rsCD40L enhanced stimulation-induced p38 MAP kinase and Akt phosphorylation.
CONCLUSION—Soluble CD40L enhances platelet activation, aggregation, and platelet-leukocyte conjugation, as well as increases stimulation-induced platelet release of RONS through activation of Akt and p38 MAP kinase signaling pathways. These data suggest that sCD40L regulates platelet-dependent inflammatory and thrombotic responses that contribute to the pathogenesis of atherothrombosis.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000184765.59207.f3</identifier><identifier>PMID: 16141403</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - metabolism ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood coagulation. Blood cells ; Blood Platelets - metabolism ; Blood vessels and receptors ; Cardiology. Vascular system ; CD40 Ligand - genetics ; CD40 Ligand - metabolism ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Fundamental and applied biological sciences. Psychology ; Medical sciences ; Mice ; Mice, Mutant Strains ; Molecular and cellular biology ; Nitric Oxide - metabolism ; Oxidative Stress - physiology ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Platelet ; Proto-Oncogene Proteins c-akt - metabolism ; Reactive Nitrogen Species - metabolism ; Reactive Oxygen Species - metabolism ; Recombinant Proteins - genetics ; Recombinant Proteins - metabolism ; Solubility ; Thrombosis - metabolism ; Vertebrates: cardiovascular system</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2428-2434</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5723-a9027ba9d03cd5d2a5ba182693d236b6fdf73a9bbefbebec95a97b68bc4662cd3</citedby><cites>FETCH-LOGICAL-c5723-a9027ba9d03cd5d2a5ba182693d236b6fdf73a9bbefbebec95a97b68bc4662cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17248051$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16141403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chakrabarti, Subrata</creatorcontrib><creatorcontrib>Varghese, Sonia</creatorcontrib><creatorcontrib>Vitseva, Olga</creatorcontrib><creatorcontrib>Tanriverdi, Kahraman</creatorcontrib><creatorcontrib>Freedman, Jane E</creatorcontrib><title>CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Soluble CD40 ligand (sCD40L) has been recently implicated in the pathogenesis of atherosclerosis. Elevated levels of sCD40L in acute coronary syndrome patients suggests enhanced platelet function; however, the exact mechanism by which this occurs is unknown. In this study, we examined the effect of sCD40L on platelet function and reactive oxygen and nitrogen species (RONS) generation.
METHODS AND RESULTS—Platelet stimulation in the presence of recombinant sCD40L (rsCD40L) led to enhanced generation of RONS as measured by DCFHDA oxidation and confocal microscopy. Incubation with rsCD40L led to enhanced platelet P-selectin expression, aggregation, and platelet-leukocyte conjugation. Platelets isolated from CD40L-deficient mice had decreased agonist-induced NO release as compared with wild-type mice. Incubation of platelets with rsCD40L enhanced stimulation-induced p38 MAP kinase and Akt phosphorylation.
CONCLUSION—Soluble CD40L enhances platelet activation, aggregation, and platelet-leukocyte conjugation, as well as increases stimulation-induced platelet release of RONS through activation of Akt and p38 MAP kinase signaling pathways. These data suggest that sCD40L regulates platelet-dependent inflammatory and thrombotic responses that contribute to the pathogenesis of atherothrombosis.</description><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood coagulation. Blood cells</subject><subject>Blood Platelets - metabolism</subject><subject>Blood vessels and receptors</subject><subject>Cardiology. Vascular system</subject><subject>CD40 Ligand - genetics</subject><subject>CD40 Ligand - metabolism</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Molecular and cellular biology</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxidative Stress - physiology</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Platelet</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Reactive Nitrogen Species - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Recombinant Proteins - genetics</subject><subject>Recombinant Proteins - metabolism</subject><subject>Solubility</subject><subject>Thrombosis - metabolism</subject><subject>Vertebrates: cardiovascular system</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkG1rFDEQgINYbK3-BVkK-m23ec_Gb-WqtnDQUqpfQ5KdtFtzu3Wza-2_d-odHBiYZAaemQkPISeMNoxpdkpZc3b7o6F4WCuNVo2ynJomiVfkiCkua6mFfo05NbZWWvJD8raUB-Ql5_QNOcQpkkkqjsjF6lzSat3f-aGrLoeUFxgilOo6-xkyzNUN3r5ANSZMfZz731Bd_Xm-gwHxGaYNdD2i5R05SD4XeL97j8n3r19uVxf1-urb5epsXUdluKi9pdwEbzsqYqc67lXwrOXaio4LHXTqkhHehgApQIBolbcm6DZEqTWPnTgmn7ZzH6fx1wJldpu-RMjZDzAuxenWCJTSInjyH_gwLtOAf3McPbTathKhz1soTmMpEyT3OPUbPz07Rt2LbEeZQ9luL9v9k-2SwOYPuw1LQA371p1dBD7uAF-iz2nyQ-zLnjNctlQx5OSWexozKi0_8_IEk7sHn-f7l9VSaKpqThFmWNYYQoi_B0qW5w</recordid><startdate>200511</startdate><enddate>200511</enddate><creator>Chakrabarti, Subrata</creator><creator>Varghese, Sonia</creator><creator>Vitseva, Olga</creator><creator>Tanriverdi, Kahraman</creator><creator>Freedman, Jane E</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>200511</creationdate><title>CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates</title><author>Chakrabarti, Subrata ; Varghese, Sonia ; Vitseva, Olga ; Tanriverdi, Kahraman ; Freedman, Jane E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5723-a9027ba9d03cd5d2a5ba182693d236b6fdf73a9bbefbebec95a97b68bc4662cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood coagulation. Blood cells</topic><topic>Blood Platelets - metabolism</topic><topic>Blood vessels and receptors</topic><topic>Cardiology. Vascular system</topic><topic>CD40 Ligand - genetics</topic><topic>CD40 Ligand - metabolism</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Molecular and cellular biology</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxidative Stress - physiology</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Platelet</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Reactive Nitrogen Species - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Recombinant Proteins - genetics</topic><topic>Recombinant Proteins - metabolism</topic><topic>Solubility</topic><topic>Thrombosis - metabolism</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chakrabarti, Subrata</creatorcontrib><creatorcontrib>Varghese, Sonia</creatorcontrib><creatorcontrib>Vitseva, Olga</creatorcontrib><creatorcontrib>Tanriverdi, Kahraman</creatorcontrib><creatorcontrib>Freedman, Jane E</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chakrabarti, Subrata</au><au>Varghese, Sonia</au><au>Vitseva, Olga</au><au>Tanriverdi, Kahraman</au><au>Freedman, Jane E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2005-11</date><risdate>2005</risdate><volume>25</volume><issue>11</issue><spage>2428</spage><epage>2434</epage><pages>2428-2434</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Soluble CD40 ligand (sCD40L) has been recently implicated in the pathogenesis of atherosclerosis. Elevated levels of sCD40L in acute coronary syndrome patients suggests enhanced platelet function; however, the exact mechanism by which this occurs is unknown. In this study, we examined the effect of sCD40L on platelet function and reactive oxygen and nitrogen species (RONS) generation.
METHODS AND RESULTS—Platelet stimulation in the presence of recombinant sCD40L (rsCD40L) led to enhanced generation of RONS as measured by DCFHDA oxidation and confocal microscopy. Incubation with rsCD40L led to enhanced platelet P-selectin expression, aggregation, and platelet-leukocyte conjugation. Platelets isolated from CD40L-deficient mice had decreased agonist-induced NO release as compared with wild-type mice. Incubation of platelets with rsCD40L enhanced stimulation-induced p38 MAP kinase and Akt phosphorylation.
CONCLUSION—Soluble CD40L enhances platelet activation, aggregation, and platelet-leukocyte conjugation, as well as increases stimulation-induced platelet release of RONS through activation of Akt and p38 MAP kinase signaling pathways. These data suggest that sCD40L regulates platelet-dependent inflammatory and thrombotic responses that contribute to the pathogenesis of atherothrombosis.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>16141403</pmid><doi>10.1161/01.ATV.0000184765.59207.f3</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2005-11, Vol.25 (11), p.2428-2434 |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Atherosclerosis (general aspects, experimental research) Atherosclerosis - metabolism Biological and medical sciences Blood and lymphatic vessels Blood coagulation. Blood cells Blood Platelets - metabolism Blood vessels and receptors Cardiology. Vascular system CD40 Ligand - genetics CD40 Ligand - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Fundamental and applied biological sciences. Psychology Medical sciences Mice Mice, Mutant Strains Molecular and cellular biology Nitric Oxide - metabolism Oxidative Stress - physiology p38 Mitogen-Activated Protein Kinases - metabolism Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Platelet Proto-Oncogene Proteins c-akt - metabolism Reactive Nitrogen Species - metabolism Reactive Oxygen Species - metabolism Recombinant Proteins - genetics Recombinant Proteins - metabolism Solubility Thrombosis - metabolism Vertebrates: cardiovascular system |
| title | CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates |
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