Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility
Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerosis susceptibility. We sought to determine whether the difference in atherosclerosis susceptibility resides at the level of arterial walls. Thoracic aortic segments from 8-week-old female B6 and C3H apolip...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2006-11, Vol.114 (22), p.2382-2389 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | HONG PEI YINONG WANG MIYOSHI, Toru ZHIMIN ZHANG MATSUMOTO, Alan H HELM, Gregory A TELLIDES, George WEIBIN SHI |
| description | Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerosis susceptibility. We sought to determine whether the difference in atherosclerosis susceptibility resides at the level of arterial walls.
Thoracic aortic segments from 8-week-old female B6 and C3H apolipoprotein E-deficient mice were transplanted into the infrarenal aorta of 10-week-old female F1 mice. After transplantation, recipients were maintained on a chow diet for 16 weeks. The donor aortic segments of B6 mice developed significantly larger atherosclerotic lesions than those of C3H (44,983+/-11,702 versus 5600+/-4885 microm2 per section; P=0.011). Expression of vascular cell adhesion molecule (VCAM)-1 by endothelial cells was examined both in vitro and in vivo. B6 mice expressed significantly more VCAM-1 than their C3H counterparts. Sequence analysis of VCAM-1 cDNA revealed a nucleotide difference in the coding region that resulted in substitution of an amino acid in the protein product.
These data provide direct proof that factors operating in the vessel wall, particularly endothelial cells, can serve as atherosclerosis modifiers and suggest a possibility for the contribution of VCAM-1 to atherosclerosis susceptibility. |
| doi_str_mv | 10.1161/circulationaha.106.640185 |
| format | Article |
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Thoracic aortic segments from 8-week-old female B6 and C3H apolipoprotein E-deficient mice were transplanted into the infrarenal aorta of 10-week-old female F1 mice. After transplantation, recipients were maintained on a chow diet for 16 weeks. The donor aortic segments of B6 mice developed significantly larger atherosclerotic lesions than those of C3H (44,983+/-11,702 versus 5600+/-4885 microm2 per section; P=0.011). Expression of vascular cell adhesion molecule (VCAM)-1 by endothelial cells was examined both in vitro and in vivo. B6 mice expressed significantly more VCAM-1 than their C3H counterparts. Sequence analysis of VCAM-1 cDNA revealed a nucleotide difference in the coding region that resulted in substitution of an amino acid in the protein product.
These data provide direct proof that factors operating in the vessel wall, particularly endothelial cells, can serve as atherosclerosis modifiers and suggest a possibility for the contribution of VCAM-1 to atherosclerosis susceptibility.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/circulationaha.106.640185</identifier><identifier>PMID: 17101850</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Aorta, Thoracic - anatomy & histology ; Aorta, Thoracic - transplantation ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - genetics ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood. Blood coagulation. Reticuloendothelial system ; Cardiology. Vascular system ; Disease Models, Animal ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Genetic Predisposition to Disease ; Lipids - blood ; Medical sciences ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Pharmacology. Drug treatments ; Transplantation, Homologous ; Vascular Cell Adhesion Molecule-1 - genetics</subject><ispartof>Circulation (New York, N.Y.), 2006-11, Vol.114 (22), p.2382-2389</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-9872f237ad5791861b25189f993f38e98d32030baffa6febacc85328bacdb2d83</citedby><cites>FETCH-LOGICAL-c505t-9872f237ad5791861b25189f993f38e98d32030baffa6febacc85328bacdb2d83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18334138$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17101850$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HONG PEI</creatorcontrib><creatorcontrib>YINONG WANG</creatorcontrib><creatorcontrib>MIYOSHI, Toru</creatorcontrib><creatorcontrib>ZHIMIN ZHANG</creatorcontrib><creatorcontrib>MATSUMOTO, Alan H</creatorcontrib><creatorcontrib>HELM, Gregory A</creatorcontrib><creatorcontrib>TELLIDES, George</creatorcontrib><creatorcontrib>WEIBIN SHI</creatorcontrib><title>Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerosis susceptibility. We sought to determine whether the difference in atherosclerosis susceptibility resides at the level of arterial walls.
Thoracic aortic segments from 8-week-old female B6 and C3H apolipoprotein E-deficient mice were transplanted into the infrarenal aorta of 10-week-old female F1 mice. After transplantation, recipients were maintained on a chow diet for 16 weeks. The donor aortic segments of B6 mice developed significantly larger atherosclerotic lesions than those of C3H (44,983+/-11,702 versus 5600+/-4885 microm2 per section; P=0.011). Expression of vascular cell adhesion molecule (VCAM)-1 by endothelial cells was examined both in vitro and in vivo. B6 mice expressed significantly more VCAM-1 than their C3H counterparts. Sequence analysis of VCAM-1 cDNA revealed a nucleotide difference in the coding region that resulted in substitution of an amino acid in the protein product.
These data provide direct proof that factors operating in the vessel wall, particularly endothelial cells, can serve as atherosclerosis modifiers and suggest a possibility for the contribution of VCAM-1 to atherosclerosis susceptibility.</description><subject>Animals</subject><subject>Aorta, Thoracic - anatomy & histology</subject><subject>Aorta, Thoracic - transplantation</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Cardiology. Vascular system</subject><subject>Disease Models, Animal</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Lipids - blood</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Pharmacology. Drug treatments</subject><subject>Transplantation, Homologous</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtLwzAUx4MoOqdfQeKDvnXmsrTJ45iXDYaC6HM5TROMZO1MUsVvb8oGvpzr71z4I3RNyYzSkt5pF_TgIbm-gw-YUVLOyjmhUhyhCRVsXswFV8doQghRRcUZO0PnMX7mtOSVOEVntKIjTiaovXfB6ITNt2tNpw22fcCAdRi0A49D7w3uLU4fBkNIJozFH_Aeuw7rvksZGPuQgdBH7UfrIo5D1GaXXOO8S78X6MSCj-by4Kfo_fHhbbkqNi9P6-ViU2hBRCqUrJhlvIJWVIrKkjZMUKmsUtxyaZRsOSOcNGAtlNY0oLUUnMkctA1rJZ-i2_3eXei_BhNTvXX5D--hM_0Q61JSRZhiGVR7UOd3YzC23gW3hfBbU1KPEtfL9evyfbN4W788L1aLXC7rvcR59upwZGi2pv2fPGiagZsDAFGDtwE67eI_JzmfUy75H04AiVQ</recordid><startdate>20061128</startdate><enddate>20061128</enddate><creator>HONG PEI</creator><creator>YINONG WANG</creator><creator>MIYOSHI, Toru</creator><creator>ZHIMIN ZHANG</creator><creator>MATSUMOTO, Alan H</creator><creator>HELM, Gregory A</creator><creator>TELLIDES, George</creator><creator>WEIBIN SHI</creator><general>Lippincott Williams & Wilkins</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>20061128</creationdate><title>Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility</title><author>HONG PEI ; YINONG WANG ; MIYOSHI, Toru ; ZHIMIN ZHANG ; MATSUMOTO, Alan H ; HELM, Gregory A ; TELLIDES, George ; WEIBIN SHI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-9872f237ad5791861b25189f993f38e98d32030baffa6febacc85328bacdb2d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Aorta, Thoracic - anatomy & histology</topic><topic>Aorta, Thoracic - transplantation</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - genetics</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Cardiology. Vascular system</topic><topic>Disease Models, Animal</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Lipids - blood</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Pharmacology. Drug treatments</topic><topic>Transplantation, Homologous</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HONG PEI</creatorcontrib><creatorcontrib>YINONG WANG</creatorcontrib><creatorcontrib>MIYOSHI, Toru</creatorcontrib><creatorcontrib>ZHIMIN ZHANG</creatorcontrib><creatorcontrib>MATSUMOTO, Alan H</creatorcontrib><creatorcontrib>HELM, Gregory A</creatorcontrib><creatorcontrib>TELLIDES, George</creatorcontrib><creatorcontrib>WEIBIN SHI</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>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HONG PEI</au><au>YINONG WANG</au><au>MIYOSHI, Toru</au><au>ZHIMIN ZHANG</au><au>MATSUMOTO, Alan H</au><au>HELM, Gregory A</au><au>TELLIDES, George</au><au>WEIBIN SHI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2006-11-28</date><risdate>2006</risdate><volume>114</volume><issue>22</issue><spage>2382</spage><epage>2389</epage><pages>2382-2389</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in atherosclerosis susceptibility. We sought to determine whether the difference in atherosclerosis susceptibility resides at the level of arterial walls.
Thoracic aortic segments from 8-week-old female B6 and C3H apolipoprotein E-deficient mice were transplanted into the infrarenal aorta of 10-week-old female F1 mice. After transplantation, recipients were maintained on a chow diet for 16 weeks. The donor aortic segments of B6 mice developed significantly larger atherosclerotic lesions than those of C3H (44,983+/-11,702 versus 5600+/-4885 microm2 per section; P=0.011). Expression of vascular cell adhesion molecule (VCAM)-1 by endothelial cells was examined both in vitro and in vivo. B6 mice expressed significantly more VCAM-1 than their C3H counterparts. Sequence analysis of VCAM-1 cDNA revealed a nucleotide difference in the coding region that resulted in substitution of an amino acid in the protein product.
These data provide direct proof that factors operating in the vessel wall, particularly endothelial cells, can serve as atherosclerosis modifiers and suggest a possibility for the contribution of VCAM-1 to atherosclerosis susceptibility.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>17101850</pmid><doi>10.1161/circulationaha.106.640185</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2006-11, Vol.114 (22), p.2382-2389 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Aorta, Thoracic - anatomy & histology Aorta, Thoracic - transplantation Apolipoproteins E - deficiency Apolipoproteins E - genetics Atherosclerosis (general aspects, experimental research) Atherosclerosis - genetics Biological and medical sciences Blood and lymphatic vessels Blood. Blood coagulation. Reticuloendothelial system Cardiology. Vascular system Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Genetic Predisposition to Disease Lipids - blood Medical sciences Mice Mice, Inbred C3H Mice, Inbred C57BL Mice, Knockout Pharmacology. Drug treatments Transplantation, Homologous Vascular Cell Adhesion Molecule-1 - genetics |
| title | Direct evidence for a crucial role of the arterial wall in control of atherosclerosis susceptibility |
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