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C-reactive protein decreases prostacyclin release from human aortic endothelial cells
In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synth...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 2003-10, Vol.108 (14), p.1676-1678 |
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| cites | cdi_FETCH-LOGICAL-c590t-b271ceb4bf76b6a7ca5825333528ec179777e1876f146623a9404cc9d06476cd3 |
| container_end_page | 1678 |
| container_issue | 14 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | SENTHIL KUMAR VENUGOPAL DEVARAJ, Sridevi JIALAL, Ishwarlal |
| description | In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs).
HAECs and HCAECs were incubated with human CRP (0 to 50 microg/mL for 24 hours). The release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease, P |
| doi_str_mv | 10.1161/01.cir.0000094736.10595.a1 |
| format | article |
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HAECs and HCAECs were incubated with human CRP (0 to 50 microg/mL for 24 hours). The release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease, P<0.001; n=5) and stimulated (26% decrease, P<0.01; n=5) conditions. CRP had no effect on PGI2 synthase (PGIS) mass. By increasing both superoxide and inducible NO synthase, CRP resulted in increased nitration of PGIS by peroxynitrite. The increased nitration and decreased activity of PGIS by CRP was reversed with peroxynitrite scavengers.
Thus, CRP decreases PGI2 release from HAECs by inactivating PGIS via nitration, additionally contributing to its atherogenicity.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.0000094736.10595.a1</identifier><identifier>PMID: 14504187</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aorta - cytology ; Aorta - metabolism ; Ascorbic Acid - pharmacology ; Biological and medical sciences ; Blood vessels and receptors ; C-Reactive Protein - pharmacology ; Cells, Cultured ; Coronary Vessels - cytology ; Coronary Vessels - metabolism ; Cytochrome P-450 Enzyme System - chemistry ; Cytochrome P-450 Enzyme System - metabolism ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Epoprostenol - biosynthesis ; Free Radical Scavengers - pharmacology ; Fundamental and applied biological sciences. Psychology ; Humans ; Intramolecular Oxidoreductases - chemistry ; Intramolecular Oxidoreductases - metabolism ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Peroxynitrous Acid - metabolism ; Prostaglandins F - biosynthesis ; Tyrosine - analogs & derivatives ; Tyrosine - analysis ; Uric Acid - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 2003-10, Vol.108 (14), p.1676-1678</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 7 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-b271ceb4bf76b6a7ca5825333528ec179777e1876f146623a9404cc9d06476cd3</citedby><cites>FETCH-LOGICAL-c590t-b271ceb4bf76b6a7ca5825333528ec179777e1876f146623a9404cc9d06476cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15193256$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14504187$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SENTHIL KUMAR VENUGOPAL</creatorcontrib><creatorcontrib>DEVARAJ, Sridevi</creatorcontrib><creatorcontrib>JIALAL, Ishwarlal</creatorcontrib><title>C-reactive protein decreases prostacyclin release from human aortic endothelial cells</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs).
HAECs and HCAECs were incubated with human CRP (0 to 50 microg/mL for 24 hours). The release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease, P<0.001; n=5) and stimulated (26% decrease, P<0.01; n=5) conditions. CRP had no effect on PGI2 synthase (PGIS) mass. By increasing both superoxide and inducible NO synthase, CRP resulted in increased nitration of PGIS by peroxynitrite. The increased nitration and decreased activity of PGIS by CRP was reversed with peroxynitrite scavengers.
Thus, CRP decreases PGI2 release from HAECs by inactivating PGIS via nitration, additionally contributing to its atherogenicity.</description><subject>Aorta - cytology</subject><subject>Aorta - metabolism</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>C-Reactive Protein - pharmacology</subject><subject>Cells, Cultured</subject><subject>Coronary Vessels - cytology</subject><subject>Coronary Vessels - metabolism</subject><subject>Cytochrome P-450 Enzyme System - chemistry</subject><subject>Cytochrome P-450 Enzyme System - metabolism</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Epoprostenol - biosynthesis</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Intramolecular Oxidoreductases - chemistry</subject><subject>Intramolecular Oxidoreductases - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Prostaglandins F - biosynthesis</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - analysis</subject><subject>Uric Acid - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNpdkF1LHTEQhkOx1FPtX5BF0LvdZvJ54p0ctBWEQtHrkJ2dxZX90GRX8N-brQcONDdD3nlm8uZl7Bx4BWDgJ4cKu1jx9ThlpamAa6erAF_YBrRQpdLSHbHN2i-tFOKYfU_pOV-NtPobOwaluYKt3bDHXRkp4Ny9UfESp5m6sWgIs5YorUqaA75jn-VI_aoWbZyG4mkZwliEKc4dFjQ20_xEfRf6Aqnv0yn72oY-0Y99PWGPtzcPu9_l_Z9fd7vr-xK143NZCwtItapba2oTLAa9FVpKqcWWEKyz1lK2aVpQxggZnOIK0TXcKGuwkSfs8nNvNvq6UJr90KXVQRhpWpK32hoJxmbw_D_weVrimL15AcI44HKboatPCPO3U6TWv8RuCPHdA_dr8p6D39399Yfk_b_k_TXk4bP9C0s9UHMY3UedgYs9EBKGvo1hxC4dOA1OCm3kB60RjDI</recordid><startdate>20031007</startdate><enddate>20031007</enddate><creator>SENTHIL KUMAR VENUGOPAL</creator><creator>DEVARAJ, Sridevi</creator><creator>JIALAL, Ishwarlal</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20031007</creationdate><title>C-reactive protein decreases prostacyclin release from human aortic endothelial cells</title><author>SENTHIL KUMAR VENUGOPAL ; DEVARAJ, Sridevi ; JIALAL, Ishwarlal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-b271ceb4bf76b6a7ca5825333528ec179777e1876f146623a9404cc9d06476cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Aorta - cytology</topic><topic>Aorta - metabolism</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>C-Reactive Protein - pharmacology</topic><topic>Cells, Cultured</topic><topic>Coronary Vessels - cytology</topic><topic>Coronary Vessels - metabolism</topic><topic>Cytochrome P-450 Enzyme System - chemistry</topic><topic>Cytochrome P-450 Enzyme System - metabolism</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Epoprostenol - biosynthesis</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Intramolecular Oxidoreductases - chemistry</topic><topic>Intramolecular Oxidoreductases - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Prostaglandins F - biosynthesis</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - analysis</topic><topic>Uric Acid - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SENTHIL KUMAR VENUGOPAL</creatorcontrib><creatorcontrib>DEVARAJ, Sridevi</creatorcontrib><creatorcontrib>JIALAL, Ishwarlal</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>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SENTHIL KUMAR VENUGOPAL</au><au>DEVARAJ, Sridevi</au><au>JIALAL, Ishwarlal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C-reactive protein decreases prostacyclin release from human aortic endothelial cells</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2003-10-07</date><risdate>2003</risdate><volume>108</volume><issue>14</issue><spage>1676</spage><epage>1678</epage><pages>1676-1678</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs).
HAECs and HCAECs were incubated with human CRP (0 to 50 microg/mL for 24 hours). The release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a potent agonist, A23187. CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease, P<0.001; n=5) and stimulated (26% decrease, P<0.01; n=5) conditions. CRP had no effect on PGI2 synthase (PGIS) mass. By increasing both superoxide and inducible NO synthase, CRP resulted in increased nitration of PGIS by peroxynitrite. The increased nitration and decreased activity of PGIS by CRP was reversed with peroxynitrite scavengers.
Thus, CRP decreases PGI2 release from HAECs by inactivating PGIS via nitration, additionally contributing to its atherogenicity.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14504187</pmid><doi>10.1161/01.cir.0000094736.10595.a1</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aorta - cytology Aorta - metabolism Ascorbic Acid - pharmacology Biological and medical sciences Blood vessels and receptors C-Reactive Protein - pharmacology Cells, Cultured Coronary Vessels - cytology Coronary Vessels - metabolism Cytochrome P-450 Enzyme System - chemistry Cytochrome P-450 Enzyme System - metabolism Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Epoprostenol - biosynthesis Free Radical Scavengers - pharmacology Fundamental and applied biological sciences. Psychology Humans Intramolecular Oxidoreductases - chemistry Intramolecular Oxidoreductases - metabolism Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Peroxynitrous Acid - metabolism Prostaglandins F - biosynthesis Tyrosine - analogs & derivatives Tyrosine - analysis Uric Acid - pharmacology Vertebrates: cardiovascular system |
| title | C-reactive protein decreases prostacyclin release from human aortic endothelial cells |
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