Lipoxygenase Products Increase Monocyte Adhesion to Human Aortic Endothelial Cells
The development of atherosclerosis is accelerated in individuals with type 2 diabetes. Adhesion of monocytes to the vascular endothelium is a key initial step in atherogenesis. We have previously shown that monocyte adhesion to human aortic endothelial cells (HAECs) cultured long-term in high-glucos...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 1999-11, Vol.19 (11), p.2615-2622 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Patricia, Mary Kim Kim, Jeong A Harper, Cynthia M Shih, Peggy T Berliner, Judith A Natarajan, Rama Nadler, Jerry L Hedrick, Catherine C |
| description | The development of atherosclerosis is accelerated in individuals with type 2 diabetes. Adhesion of monocytes to the vascular endothelium is a key initial step in atherogenesis. We have previously shown that monocyte adhesion to human aortic endothelial cells (HAECs) cultured long-term in high-glucose medium (25 mmol/L, 2 passages) is increased compared with cells grown in normal glucose (5 mmol/L). One potential mechanism for increased monocyte adhesion to HAECs under hyperglycemic conditions is via the 12-lipoxygenase (12-LO) pathway. In this study, we demonstrated in HAECs that the major LO metabolite of arachidonic acid was the 12-LO product, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], which was increased severalfold in HAECs cultured under high-glucose conditions. Furthermore, treatment of HAECs with 12(S)-HETE induced monocyte, but not neutrophil, adhesion an average of 3-fold (range of 1.5- to 5-fold) compared with untreated cells (75±5 versus 26±1 monocytes per field, respectively, P |
| doi_str_mv | 10.1161/01.atv.19.11.2615 |
| format | Article |
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Adhesion of monocytes to the vascular endothelium is a key initial step in atherogenesis. We have previously shown that monocyte adhesion to human aortic endothelial cells (HAECs) cultured long-term in high-glucose medium (25 mmol/L, 2 passages) is increased compared with cells grown in normal glucose (5 mmol/L). One potential mechanism for increased monocyte adhesion to HAECs under hyperglycemic conditions is via the 12-lipoxygenase (12-LO) pathway. In this study, we demonstrated in HAECs that the major LO metabolite of arachidonic acid was the 12-LO product, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], which was increased severalfold in HAECs cultured under high-glucose conditions. Furthermore, treatment of HAECs with 12(S)-HETE induced monocyte, but not neutrophil, adhesion an average of 3-fold (range of 1.5- to 5-fold) compared with untreated cells (75±5 versus 26±1 monocytes per field, respectively, P<0.001). Expression of the adhesion molecules vascular cell adhesion molecule-1, E-selectin, and intercellular adhesion molecule-1 was not significantly increased. However, both glucose and 12(S)-HETE induced a 60% increase in HAEC surface expression of connecting segment-1 (ie, CS-1) fibronectin, a ligand for very late-acting antigen-4 (VLA-4). The antibodies used to block monocyte integrin VLA-4 and leukocyte function-related antigen-1, a monocytic counterreceptor for intercellular adhesion molecule-1, inhibited the ability of both 12-LO products and high glucose to induce monocyte adhesion. These results definitively demonstrate for the first time in HAECs that the 12-LO pathway can induce monocyte-endothelial cell interaction and that the effects of glucose may be mediated, at least in part, through this pathway. Thus, these results suggest that the 12-LO pathway may play a role in the increased susceptibility of diabetics to atherosclerosis.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.atv.19.11.2615</identifier><identifier>PMID: 10559003</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - biosynthesis ; 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - pharmacology ; Antibodies, Blocking ; Antigens, CD - immunology ; Antigens, CD - metabolism ; Aorta - cytology ; Arteriosclerosis - enzymology ; Associated diseases and complications ; Biological and medical sciences ; CD18 Antigens - immunology ; CD18 Antigens - metabolism ; Cell Adhesion - drug effects ; Cell Adhesion - physiology ; Cells, Cultured ; Diabetes. Impaired glucose tolerance ; E-Selectin - metabolism ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - enzymology ; Glucose - pharmacology ; Humans ; Hydroxyeicosatetraenoic Acids - pharmacology ; Hyperglycemia - enzymology ; Integrin alpha4 ; Intercellular Adhesion Molecule-1 - immunology ; Intercellular Adhesion Molecule-1 - metabolism ; Lipoxygenase - metabolism ; Medical sciences ; Monocytes - cytology ; Neutrophils - cytology ; Neutrophils - drug effects ; Vascular Cell Adhesion Molecule-1 - metabolism</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 1999-11, Vol.19 (11), p.2615-2622</ispartof><rights>1999 American Heart Association, Inc.</rights><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5906-ceb6ca792d9a869aad5c3c4c2834aaf04cea93966bf651e503eb7783cacbb1223</citedby><cites>FETCH-LOGICAL-c5906-ceb6ca792d9a869aad5c3c4c2834aaf04cea93966bf651e503eb7783cacbb1223</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=1198908$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10559003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Patricia, Mary Kim</creatorcontrib><creatorcontrib>Kim, Jeong A</creatorcontrib><creatorcontrib>Harper, Cynthia M</creatorcontrib><creatorcontrib>Shih, Peggy T</creatorcontrib><creatorcontrib>Berliner, Judith A</creatorcontrib><creatorcontrib>Natarajan, Rama</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><creatorcontrib>Hedrick, Catherine C</creatorcontrib><title>Lipoxygenase Products Increase Monocyte Adhesion to Human Aortic Endothelial Cells</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>The development of atherosclerosis is accelerated in individuals with type 2 diabetes. Adhesion of monocytes to the vascular endothelium is a key initial step in atherogenesis. We have previously shown that monocyte adhesion to human aortic endothelial cells (HAECs) cultured long-term in high-glucose medium (25 mmol/L, 2 passages) is increased compared with cells grown in normal glucose (5 mmol/L). One potential mechanism for increased monocyte adhesion to HAECs under hyperglycemic conditions is via the 12-lipoxygenase (12-LO) pathway. In this study, we demonstrated in HAECs that the major LO metabolite of arachidonic acid was the 12-LO product, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], which was increased severalfold in HAECs cultured under high-glucose conditions. Furthermore, treatment of HAECs with 12(S)-HETE induced monocyte, but not neutrophil, adhesion an average of 3-fold (range of 1.5- to 5-fold) compared with untreated cells (75±5 versus 26±1 monocytes per field, respectively, P<0.001). Expression of the adhesion molecules vascular cell adhesion molecule-1, E-selectin, and intercellular adhesion molecule-1 was not significantly increased. However, both glucose and 12(S)-HETE induced a 60% increase in HAEC surface expression of connecting segment-1 (ie, CS-1) fibronectin, a ligand for very late-acting antigen-4 (VLA-4). The antibodies used to block monocyte integrin VLA-4 and leukocyte function-related antigen-1, a monocytic counterreceptor for intercellular adhesion molecule-1, inhibited the ability of both 12-LO products and high glucose to induce monocyte adhesion. These results definitively demonstrate for the first time in HAECs that the 12-LO pathway can induce monocyte-endothelial cell interaction and that the effects of glucose may be mediated, at least in part, through this pathway. Thus, these results suggest that the 12-LO pathway may play a role in the increased susceptibility of diabetics to atherosclerosis.</description><subject>12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - biosynthesis</subject><subject>12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - pharmacology</subject><subject>Antibodies, Blocking</subject><subject>Antigens, CD - immunology</subject><subject>Antigens, CD - metabolism</subject><subject>Aorta - cytology</subject><subject>Arteriosclerosis - enzymology</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>CD18 Antigens - immunology</subject><subject>CD18 Antigens - metabolism</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Adhesion - physiology</subject><subject>Cells, Cultured</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>E-Selectin - metabolism</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Glucose - pharmacology</subject><subject>Humans</subject><subject>Hydroxyeicosatetraenoic Acids - pharmacology</subject><subject>Hyperglycemia - enzymology</subject><subject>Integrin alpha4</subject><subject>Intercellular Adhesion Molecule-1 - immunology</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Lipoxygenase - metabolism</subject><subject>Medical sciences</subject><subject>Monocytes - cytology</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - drug effects</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFv1DAQhSMEoqXwA7igCFXcsnjs2ImPq1WhlRaBUOFqTZwJm-K1Fzuh7L_H212piIM1ftY3z6M3RfEa2AJAwXsGC5x-L0BnueAK5JPiHCSvq1oJ9TTfWaMrqWp-VrxI6Y4xVnPOnhdnwKTUjInz4ut63IU_-x_kMVH5JYZ-tlMqb7yNdHj5FHyw-4nKZb-hNAZfTqG8nrfoy2WI02jLK9-HaUNuRFeuyLn0sng2oEv06lQvim8frm5X19X688eb1XJd2fy3qix1ymKjea-xVRqxl1bY2vJW1IgDqy2hFlqpblASSDJBXdO0wqLtOuBcXBTvjr67GH7NlCazHZPNE6CnMCejNG-UFCyDb_8D78IcfZ7N8JyIhvbBDY6QjSGlSIPZxXGLcW-AmUPahoFZ3n43oLM0h7Rzz5uT8dxtqf-n4xhvBi5PACaLbojo7ZgeOdCtZm3G6iN2H9xEMf108z1FsyF008Yc1iYUkxVorQGyrPJhSvwFShyXPw</recordid><startdate>199911</startdate><enddate>199911</enddate><creator>Patricia, Mary Kim</creator><creator>Kim, Jeong A</creator><creator>Harper, Cynthia M</creator><creator>Shih, Peggy T</creator><creator>Berliner, Judith A</creator><creator>Natarajan, Rama</creator><creator>Nadler, Jerry L</creator><creator>Hedrick, Catherine C</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>199911</creationdate><title>Lipoxygenase Products Increase Monocyte Adhesion to Human Aortic Endothelial Cells</title><author>Patricia, Mary Kim ; Kim, Jeong A ; Harper, Cynthia M ; Shih, Peggy T ; Berliner, Judith A ; Natarajan, Rama ; Nadler, Jerry L ; Hedrick, Catherine C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5906-ceb6ca792d9a869aad5c3c4c2834aaf04cea93966bf651e503eb7783cacbb1223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - biosynthesis</topic><topic>12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - pharmacology</topic><topic>Antibodies, Blocking</topic><topic>Antigens, CD - immunology</topic><topic>Antigens, CD - metabolism</topic><topic>Aorta - cytology</topic><topic>Arteriosclerosis - enzymology</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>CD18 Antigens - immunology</topic><topic>CD18 Antigens - metabolism</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Adhesion - physiology</topic><topic>Cells, Cultured</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>E-Selectin - metabolism</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Glucose - pharmacology</topic><topic>Humans</topic><topic>Hydroxyeicosatetraenoic Acids - pharmacology</topic><topic>Hyperglycemia - enzymology</topic><topic>Integrin alpha4</topic><topic>Intercellular Adhesion Molecule-1 - immunology</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Lipoxygenase - metabolism</topic><topic>Medical sciences</topic><topic>Monocytes - cytology</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - drug effects</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patricia, Mary Kim</creatorcontrib><creatorcontrib>Kim, Jeong A</creatorcontrib><creatorcontrib>Harper, Cynthia M</creatorcontrib><creatorcontrib>Shih, Peggy T</creatorcontrib><creatorcontrib>Berliner, Judith A</creatorcontrib><creatorcontrib>Natarajan, Rama</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><creatorcontrib>Hedrick, Catherine C</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>Patricia, Mary Kim</au><au>Kim, Jeong A</au><au>Harper, Cynthia M</au><au>Shih, Peggy T</au><au>Berliner, Judith A</au><au>Natarajan, Rama</au><au>Nadler, Jerry L</au><au>Hedrick, Catherine C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipoxygenase Products Increase Monocyte Adhesion to Human Aortic Endothelial Cells</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>1999-11</date><risdate>1999</risdate><volume>19</volume><issue>11</issue><spage>2615</spage><epage>2622</epage><pages>2615-2622</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>The development of atherosclerosis is accelerated in individuals with type 2 diabetes. Adhesion of monocytes to the vascular endothelium is a key initial step in atherogenesis. We have previously shown that monocyte adhesion to human aortic endothelial cells (HAECs) cultured long-term in high-glucose medium (25 mmol/L, 2 passages) is increased compared with cells grown in normal glucose (5 mmol/L). One potential mechanism for increased monocyte adhesion to HAECs under hyperglycemic conditions is via the 12-lipoxygenase (12-LO) pathway. In this study, we demonstrated in HAECs that the major LO metabolite of arachidonic acid was the 12-LO product, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], which was increased severalfold in HAECs cultured under high-glucose conditions. Furthermore, treatment of HAECs with 12(S)-HETE induced monocyte, but not neutrophil, adhesion an average of 3-fold (range of 1.5- to 5-fold) compared with untreated cells (75±5 versus 26±1 monocytes per field, respectively, P<0.001). Expression of the adhesion molecules vascular cell adhesion molecule-1, E-selectin, and intercellular adhesion molecule-1 was not significantly increased. However, both glucose and 12(S)-HETE induced a 60% increase in HAEC surface expression of connecting segment-1 (ie, CS-1) fibronectin, a ligand for very late-acting antigen-4 (VLA-4). The antibodies used to block monocyte integrin VLA-4 and leukocyte function-related antigen-1, a monocytic counterreceptor for intercellular adhesion molecule-1, inhibited the ability of both 12-LO products and high glucose to induce monocyte adhesion. These results definitively demonstrate for the first time in HAECs that the 12-LO pathway can induce monocyte-endothelial cell interaction and that the effects of glucose may be mediated, at least in part, through this pathway. Thus, these results suggest that the 12-LO pathway may play a role in the increased susceptibility of diabetics to atherosclerosis.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>10559003</pmid><doi>10.1161/01.atv.19.11.2615</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 1999-11, Vol.19 (11), p.2615-2622 |
| issn | 1079-5642 1524-4636 |
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| subjects | 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - biosynthesis 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid - pharmacology Antibodies, Blocking Antigens, CD - immunology Antigens, CD - metabolism Aorta - cytology Arteriosclerosis - enzymology Associated diseases and complications Biological and medical sciences CD18 Antigens - immunology CD18 Antigens - metabolism Cell Adhesion - drug effects Cell Adhesion - physiology Cells, Cultured Diabetes. Impaired glucose tolerance E-Selectin - metabolism Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - enzymology Glucose - pharmacology Humans Hydroxyeicosatetraenoic Acids - pharmacology Hyperglycemia - enzymology Integrin alpha4 Intercellular Adhesion Molecule-1 - immunology Intercellular Adhesion Molecule-1 - metabolism Lipoxygenase - metabolism Medical sciences Monocytes - cytology Neutrophils - cytology Neutrophils - drug effects Vascular Cell Adhesion Molecule-1 - metabolism |
| title | Lipoxygenase Products Increase Monocyte Adhesion to Human Aortic Endothelial Cells |
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