Changes in markers of vascular injury in response to transient hyperhomocysteinemia
The purpose of this study was to test whether transient increases in homocysteine would promote changes in markers of endothelial injury, cellular fibronectin (cFN), and soluble vascular cell adhesion molecule 1 (sVCAM-1). Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in resp...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2003-04, Vol.52 (4), p.501-507 |
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| container_title | Metabolism, clinical and experimental |
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| creator | Powers, Robert W. Majors, Alana K. Cerula, Stacy L. Huber, Heather A. Schmidt, Brian P. Roberts, James M. |
| description | The purpose of this study was to test whether transient increases in homocysteine would promote changes in markers of endothelial injury, cellular fibronectin (cFN), and soluble vascular cell adhesion molecule 1 (sVCAM-1). Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in response to a methionine load by 6 hours in human subjects. However, no correlation was observed between homocysteine and cFN or sVCAM-1. To directly test whether homocysteine can injure endothelial cells, human umbilical vein endothelial cells (HUVEC) were incubated with increasing concentrations of homocysteine, plasma, or serum from hyperhomocysteinemic mice or from the methionine-loaded test subjects. cFN release was increased from endothelial cells cultured with plasma (but not serum) of hyperhomocysteinemic transgenic mice or from methionine-loaded human subjects. These data suggest that very high homocysteine concentrations can promote endothelial injury; however, this effect is likely mediated by secondary effects that include a factor(s) present in plasma that affects endothelial cells. Copyright 2003 Elsevier, Inc. All rights reserved. |
| doi_str_mv | 10.1053/meta.2003.50081 |
| format | Article |
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Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in response to a methionine load by 6 hours in human subjects. However, no correlation was observed between homocysteine and cFN or sVCAM-1. To directly test whether homocysteine can injure endothelial cells, human umbilical vein endothelial cells (HUVEC) were incubated with increasing concentrations of homocysteine, plasma, or serum from hyperhomocysteinemic mice or from the methionine-loaded test subjects. cFN release was increased from endothelial cells cultured with plasma (but not serum) of hyperhomocysteinemic transgenic mice or from methionine-loaded human subjects. These data suggest that very high homocysteine concentrations can promote endothelial injury; however, this effect is likely mediated by secondary effects that include a factor(s) present in plasma that affects endothelial cells. Copyright 2003 Elsevier, Inc. All rights reserved.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1053/meta.2003.50081</identifier><identifier>PMID: 12701066</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Animals ; Biological and medical sciences ; Biomarkers ; Blood and lymphatic vessels ; Blood Vessels - pathology ; Cardiology. Vascular system ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Enzyme-Linked Immunosorbent Assay ; Female ; Fibronectins - blood ; Homocysteine - blood ; Humans ; Hyperhomocysteinemia - blood ; Hyperhomocysteinemia - genetics ; Hyperhomocysteinemia - pathology ; Male ; Medical sciences ; Methionine - pharmacology ; Mice ; Mice, Transgenic ; Vascular Cell Adhesion Molecule-1 - blood</subject><ispartof>Metabolism, clinical and experimental, 2003-04, Vol.52 (4), p.501-507</ispartof><rights>2003 Elsevier Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2003 Elsevier, Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-962e9bc199bf9f1f4434bdd957fee3f942d80585cd1e9b69812a4210304b88da3</citedby><cites>FETCH-LOGICAL-c373t-962e9bc199bf9f1f4434bdd957fee3f942d80585cd1e9b69812a4210304b88da3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0026049502052903$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14737183$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12701066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Powers, Robert W.</creatorcontrib><creatorcontrib>Majors, Alana K.</creatorcontrib><creatorcontrib>Cerula, Stacy L.</creatorcontrib><creatorcontrib>Huber, Heather A.</creatorcontrib><creatorcontrib>Schmidt, Brian P.</creatorcontrib><creatorcontrib>Roberts, James M.</creatorcontrib><title>Changes in markers of vascular injury in response to transient hyperhomocysteinemia</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>The purpose of this study was to test whether transient increases in homocysteine would promote changes in markers of endothelial injury, cellular fibronectin (cFN), and soluble vascular cell adhesion molecule 1 (sVCAM-1). Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in response to a methionine load by 6 hours in human subjects. However, no correlation was observed between homocysteine and cFN or sVCAM-1. To directly test whether homocysteine can injure endothelial cells, human umbilical vein endothelial cells (HUVEC) were incubated with increasing concentrations of homocysteine, plasma, or serum from hyperhomocysteinemic mice or from the methionine-loaded test subjects. cFN release was increased from endothelial cells cultured with plasma (but not serum) of hyperhomocysteinemic transgenic mice or from methionine-loaded human subjects. These data suggest that very high homocysteine concentrations can promote endothelial injury; however, this effect is likely mediated by secondary effects that include a factor(s) present in plasma that affects endothelial cells. Copyright 2003 Elsevier, Inc. All rights reserved.</description><subject>Adult</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Vessels - pathology</subject><subject>Cardiology. Vascular system</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Fibronectins - blood</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - blood</subject><subject>Hyperhomocysteinemia - genetics</subject><subject>Hyperhomocysteinemia - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methionine - pharmacology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Vascular Cell Adhesion Molecule-1 - blood</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10E1v3CAQgGFUpWo2ac-5Rb6kN28G8Acco1X6IUXqoe0ZYTxkSWyzYexI--_LdlfKKSckeBjBy9gVhzWHWt6OONu1AJDrGkDxD2zFaylK1QCcsRWAaEqodH3OLoieAKBtVfOJnXPRAoemWbHfm62dHpGKMBWjTc-YqIi-eLXklsGmvP20pP3hNCHt4kRYzLGYk50o4DQX2_0O0zaO0e1pxjDhGOxn9tHbgfDLab1kf7_d_9n8KB9-ff-5uXsonWzlXOpGoO4c17rz2nNfVbLq-l7XrUeUXleiV1Cr2vU8u0YrLmwlOEioOqV6Ky_Z1-PcXYovC9JsxkAOh8FOGBcyrRRCKAUZ3h6hS5EooTe7FPJv94aDOXQ0h47m0NH875hvXJ9GL92I_Zs_hcvg5gRyKTv4HMQFenNVK1uuZHb66DCHeA2YDLkczmEfErrZ9DG8-4h_UCmPww</recordid><startdate>20030401</startdate><enddate>20030401</enddate><creator>Powers, Robert W.</creator><creator>Majors, Alana K.</creator><creator>Cerula, Stacy L.</creator><creator>Huber, Heather A.</creator><creator>Schmidt, Brian P.</creator><creator>Roberts, James M.</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>20030401</creationdate><title>Changes in markers of vascular injury in response to transient hyperhomocysteinemia</title><author>Powers, Robert W. ; Majors, Alana K. ; Cerula, Stacy L. ; Huber, Heather A. ; Schmidt, Brian P. ; Roberts, James M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-962e9bc199bf9f1f4434bdd957fee3f942d80585cd1e9b69812a4210304b88da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Vessels - pathology</topic><topic>Cardiology. Vascular system</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Fibronectins - blood</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - blood</topic><topic>Hyperhomocysteinemia - genetics</topic><topic>Hyperhomocysteinemia - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methionine - pharmacology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Vascular Cell Adhesion Molecule-1 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Powers, Robert W.</creatorcontrib><creatorcontrib>Majors, Alana K.</creatorcontrib><creatorcontrib>Cerula, Stacy L.</creatorcontrib><creatorcontrib>Huber, Heather A.</creatorcontrib><creatorcontrib>Schmidt, Brian P.</creatorcontrib><creatorcontrib>Roberts, James M.</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>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Powers, Robert W.</au><au>Majors, Alana K.</au><au>Cerula, Stacy L.</au><au>Huber, Heather A.</au><au>Schmidt, Brian P.</au><au>Roberts, James M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in markers of vascular injury in response to transient hyperhomocysteinemia</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2003-04-01</date><risdate>2003</risdate><volume>52</volume><issue>4</issue><spage>501</spage><epage>507</epage><pages>501-507</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>The purpose of this study was to test whether transient increases in homocysteine would promote changes in markers of endothelial injury, cellular fibronectin (cFN), and soluble vascular cell adhesion molecule 1 (sVCAM-1). Homocysteine, cFN, and sVCAM-1 concentrations increased significantly in response to a methionine load by 6 hours in human subjects. However, no correlation was observed between homocysteine and cFN or sVCAM-1. To directly test whether homocysteine can injure endothelial cells, human umbilical vein endothelial cells (HUVEC) were incubated with increasing concentrations of homocysteine, plasma, or serum from hyperhomocysteinemic mice or from the methionine-loaded test subjects. cFN release was increased from endothelial cells cultured with plasma (but not serum) of hyperhomocysteinemic transgenic mice or from methionine-loaded human subjects. These data suggest that very high homocysteine concentrations can promote endothelial injury; however, this effect is likely mediated by secondary effects that include a factor(s) present in plasma that affects endothelial cells. Copyright 2003 Elsevier, Inc. All rights reserved.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12701066</pmid><doi>10.1053/meta.2003.50081</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Animals Biological and medical sciences Biomarkers Blood and lymphatic vessels Blood Vessels - pathology Cardiology. Vascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Enzyme-Linked Immunosorbent Assay Female Fibronectins - blood Homocysteine - blood Humans Hyperhomocysteinemia - blood Hyperhomocysteinemia - genetics Hyperhomocysteinemia - pathology Male Medical sciences Methionine - pharmacology Mice Mice, Transgenic Vascular Cell Adhesion Molecule-1 - blood |
| title | Changes in markers of vascular injury in response to transient hyperhomocysteinemia |
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