Expression of Multiple Isoforms of Nitric Oxide Synthase in Normal and Atherosclerotic Vessels
Atherosclerosis is associated with reduced endothelium-derived relaxing factor bioactivity. To determine whether this is due to decreased synthesis of nitric oxide synthase (NOS), we examined normal and atherosclerotic human vessels by in situ hybridization and immunocytochemistry by using probes sp...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 1997-11, Vol.17 (11), p.2479-2488 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Wilcox, Josiah N Subramanian, Romesh R Sundell, Cynthia L Tracey, W. Ross Pollock, Jennifer S Harrison, David G Marsden, Philip A |
| description | Atherosclerosis is associated with reduced endothelium-derived relaxing factor bioactivity. To determine whether this is due to decreased synthesis of nitric oxide synthase (NOS), we examined normal and atherosclerotic human vessels by in situ hybridization and immunocytochemistry by using probes specific for endothelial (ecNOS), inducible (iNOS), and neuronal (nNOS) NOS isoforms. ecNOS was detected in endothelial cells overlying normal human aortas, fatty streaks, and advanced atherosclerotic lesions. A comparison of the relative expression of ecNOS to von Willebrand factor on serial sections of normal and atherosclerotic vessels indicated that there was a decrease in the number of endothelial cells expressing ecNOS in advanced lesions. iNOS and nNOS were not detected in normal vessels, but widespread production of these isoforms was found in early and advanced lesions associated with macrophages, endothelial cells, and mesenchymal-appearing intimal cells. These data suggest that there is (1) a loss of ecNOS expression by endothelial cells over advanced atherosclerotic lesions and (2) a significant increase in overall NOS synthesis by other cell types in advanced lesions composed of the ecNOS, nNOS, and iNOS isoforms. We hypothesize that the increased expression of NOS and presumably NO in atherosclerotic plaques may be related to cell death and necrosis in these tissues. (Arterioscler Thromb Vasc Biol. 1997;17:2479-2488.) |
| doi_str_mv | 10.1161/01.atv.17.11.2479 |
| format | Article |
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A comparison of the relative expression of ecNOS to von Willebrand factor on serial sections of normal and atherosclerotic vessels indicated that there was a decrease in the number of endothelial cells expressing ecNOS in advanced lesions. iNOS and nNOS were not detected in normal vessels, but widespread production of these isoforms was found in early and advanced lesions associated with macrophages, endothelial cells, and mesenchymal-appearing intimal cells. These data suggest that there is (1) a loss of ecNOS expression by endothelial cells over advanced atherosclerotic lesions and (2) a significant increase in overall NOS synthesis by other cell types in advanced lesions composed of the ecNOS, nNOS, and iNOS isoforms. We hypothesize that the increased expression of NOS and presumably NO in atherosclerotic plaques may be related to cell death and necrosis in these tissues. (Arterioscler Thromb Vasc Biol. 1997;17:2479-2488.)</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.atv.17.11.2479</identifier><identifier>PMID: 9409218</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging - metabolism ; Aorta - enzymology ; Aorta - growth & development ; Aorta - pathology ; Arteriosclerosis - enzymology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Carotid Stenosis - enzymology ; Carotid Stenosis - pathology ; Child ; Endothelium, Vascular - enzymology ; Female ; Gene Expression Regulation, Enzymologic ; Humans ; Immunoenzyme Techniques ; In Situ Hybridization ; Isoenzymes - biosynthesis ; Isoenzymes - genetics ; Macrophages - enzymology ; Male ; Medical sciences ; Middle Aged ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase - genetics ; Vasa Vasorum - enzymology</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 1997-11, Vol.17 (11), p.2479-2488</ispartof><rights>1997 American Heart Association, Inc.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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Ross</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Harrison, David G</creatorcontrib><creatorcontrib>Marsden, Philip A</creatorcontrib><title>Expression of Multiple Isoforms of Nitric Oxide Synthase in Normal and Atherosclerotic Vessels</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>Atherosclerosis is associated with reduced endothelium-derived relaxing factor bioactivity. To determine whether this is due to decreased synthesis of nitric oxide synthase (NOS), we examined normal and atherosclerotic human vessels by in situ hybridization and immunocytochemistry by using probes specific for endothelial (ecNOS), inducible (iNOS), and neuronal (nNOS) NOS isoforms. ecNOS was detected in endothelial cells overlying normal human aortas, fatty streaks, and advanced atherosclerotic lesions. A comparison of the relative expression of ecNOS to von Willebrand factor on serial sections of normal and atherosclerotic vessels indicated that there was a decrease in the number of endothelial cells expressing ecNOS in advanced lesions. iNOS and nNOS were not detected in normal vessels, but widespread production of these isoforms was found in early and advanced lesions associated with macrophages, endothelial cells, and mesenchymal-appearing intimal cells. These data suggest that there is (1) a loss of ecNOS expression by endothelial cells over advanced atherosclerotic lesions and (2) a significant increase in overall NOS synthesis by other cell types in advanced lesions composed of the ecNOS, nNOS, and iNOS isoforms. We hypothesize that the increased expression of NOS and presumably NO in atherosclerotic plaques may be related to cell death and necrosis in these tissues. (Arterioscler Thromb Vasc Biol. 1997;17:2479-2488.)</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - metabolism</subject><subject>Aorta - enzymology</subject><subject>Aorta - growth & development</subject><subject>Aorta - pathology</subject><subject>Arteriosclerosis - enzymology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Stenosis - enzymology</subject><subject>Carotid Stenosis - pathology</subject><subject>Child</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Female</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>In Situ Hybridization</subject><subject>Isoenzymes - biosynthesis</subject><subject>Isoenzymes - genetics</subject><subject>Macrophages - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Vasa Vasorum - enzymology</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVFvFCEQx4nR1Hr6AXww2ZjGtz0ZloXl8dJUbVLbB2sfJSw35KjccgJr228vl7v0wQdghvnNP_AfQt4DXQII-ExhacrfJciaLhmX6gU5hZ7xlotOvKwxlartBWevyZuc7ymlnDF6Qk4Up4rBcEp-XTzuEubs49RE13yfQ_G7gM1lji6mbd5fXvuSvG1uHv0amx9PU9mYjI2fmutKmNCYad2sygZTzDbUvVT4rmpiyG_JK2dCxnfHc0F-frm4Pf_WXt18vTxfXbW2HxRv3TBa2TsYjGNsZLYbhQRBkTrqcEA7jtgpNTBj0CmGApUSzKwZds464H23IJ8OursU_8yYi976bDEEM2Gcs5aKK8Ypq-DH_8D7OKepvk2zao6ispMVggNk65dyQqd3yW9NetJA9d54TUGvbu80yJrqvfG158NReB63uH7uODpd62fHusnWBJfMZH1-xhhQQevUFoQfsIcYCqb8O8wPmPQGTSgbvR9gJ2jfglISoKZtXYx3_wBQiZvF</recordid><startdate>199711</startdate><enddate>199711</enddate><creator>Wilcox, Josiah N</creator><creator>Subramanian, Romesh R</creator><creator>Sundell, Cynthia L</creator><creator>Tracey, W. Ross</creator><creator>Pollock, Jennifer S</creator><creator>Harrison, David G</creator><creator>Marsden, Philip A</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>199711</creationdate><title>Expression of Multiple Isoforms of Nitric Oxide Synthase in Normal and Atherosclerotic Vessels</title><author>Wilcox, Josiah N ; Subramanian, Romesh R ; Sundell, Cynthia L ; Tracey, W. Ross ; Pollock, Jennifer S ; Harrison, David G ; Marsden, Philip A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5894-f8bc75f18af22b2c3b67160e0f0fe8ecbbe39982aaef92e6e9962ad2e3fcf1453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - metabolism</topic><topic>Aorta - enzymology</topic><topic>Aorta - growth & development</topic><topic>Aorta - pathology</topic><topic>Arteriosclerosis - enzymology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Stenosis - enzymology</topic><topic>Carotid Stenosis - pathology</topic><topic>Child</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Female</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>In Situ Hybridization</topic><topic>Isoenzymes - biosynthesis</topic><topic>Isoenzymes - genetics</topic><topic>Macrophages - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Vasa Vasorum - enzymology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wilcox, Josiah N</creatorcontrib><creatorcontrib>Subramanian, Romesh R</creatorcontrib><creatorcontrib>Sundell, Cynthia L</creatorcontrib><creatorcontrib>Tracey, W. Ross</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Harrison, David G</creatorcontrib><creatorcontrib>Marsden, Philip A</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>Wilcox, Josiah N</au><au>Subramanian, Romesh R</au><au>Sundell, Cynthia L</au><au>Tracey, W. 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To determine whether this is due to decreased synthesis of nitric oxide synthase (NOS), we examined normal and atherosclerotic human vessels by in situ hybridization and immunocytochemistry by using probes specific for endothelial (ecNOS), inducible (iNOS), and neuronal (nNOS) NOS isoforms. ecNOS was detected in endothelial cells overlying normal human aortas, fatty streaks, and advanced atherosclerotic lesions. A comparison of the relative expression of ecNOS to von Willebrand factor on serial sections of normal and atherosclerotic vessels indicated that there was a decrease in the number of endothelial cells expressing ecNOS in advanced lesions. iNOS and nNOS were not detected in normal vessels, but widespread production of these isoforms was found in early and advanced lesions associated with macrophages, endothelial cells, and mesenchymal-appearing intimal cells. These data suggest that there is (1) a loss of ecNOS expression by endothelial cells over advanced atherosclerotic lesions and (2) a significant increase in overall NOS synthesis by other cell types in advanced lesions composed of the ecNOS, nNOS, and iNOS isoforms. We hypothesize that the increased expression of NOS and presumably NO in atherosclerotic plaques may be related to cell death and necrosis in these tissues. (Arterioscler Thromb Vasc Biol. 1997;17:2479-2488.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9409218</pmid><doi>10.1161/01.atv.17.11.2479</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 1997-11, Vol.17 (11), p.2479-2488 |
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| subjects | Adolescent Adult Aged Aged, 80 and over Aging - metabolism Aorta - enzymology Aorta - growth & development Aorta - pathology Arteriosclerosis - enzymology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Carotid Stenosis - enzymology Carotid Stenosis - pathology Child Endothelium, Vascular - enzymology Female Gene Expression Regulation, Enzymologic Humans Immunoenzyme Techniques In Situ Hybridization Isoenzymes - biosynthesis Isoenzymes - genetics Macrophages - enzymology Male Medical sciences Middle Aged Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase - genetics Vasa Vasorum - enzymology |
| title | Expression of Multiple Isoforms of Nitric Oxide Synthase in Normal and Atherosclerotic Vessels |
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