Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas
To better understand the morphogenesis of atherosclerotic plaque, we evaluated temporal distribution of leukocytes, macrophages, foam cells, vascular smooth muscle cells, and subendothelial lipid in Watanabe heritable hyperlipedimic (WHHL) rabbit aortas. Aortas of WHHL (n=20) and New Zealand White (...
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| Veröffentlicht in: | Cardiovascular pathology 2001-01, Vol.10 (1), p.1-11 |
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| creator | Clubb, Fred J Cerny, Jeff L Deferrari, Dario A Butler-Aucoin, Michelle M Willerson, James T Buja, L.Maximilian |
| description | To better understand the morphogenesis of atherosclerotic plaque, we evaluated temporal distribution of leukocytes, macrophages, foam cells, vascular smooth muscle cells, and subendothelial lipid in Watanabe heritable hyperlipedimic (WHHL) rabbit aortas. Aortas of WHHL (n=20) and New Zealand White (NZW, controls; n=8) rabbits were perfusion fixed at 1, 3, 6, and 12 months of age. At initial gross evaluation of lipid distribution, we identified aortic areas at high risk for lesion development. In WHHL rabbits, the lipid-positive portion of high-risk areas increased from 3% at 1 month to 50% at 12 months; during the same period, adherent cell count increased from |
| doi_str_mv | 10.1016/S1054-8807(00)00054-5 |
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2 to 25 leukocytes, 44 monocytes, and 10 foam cells/mm
2. Controls showed no increase over time in lipid-positive areas or cellular adherence to the endothelium. One-month-old WHHL rabbit aortas had scattered lipid-positive cells in the intima (primarily branch points). Immunostaining of these areas did not show rabbit macrophages (RAM antibody) but were actin positive. Occasionally, platelets and monocytes adhered to the endothelial surface. By age 3 months, well-defined fatty streaks/atherosclerotic plaques had RAM-positive cells within foam cell core, along core margins, and in focal clusters in the fibrous cap and subendothelium. By age 12 months, isolated RAM-positive cells were on the endothelial surface, and surface morphology showed endothelial cell disruption foci containing clusters of macrophages and foam cells. Our results indicate that lipid accumulation (extra- and intracellular) is important in the early development of atherosclerotic lesions; a corresponding, slower accumulation of adherent cells on the lesion surface promotes lipid conversion from fatty streak to plaque.</description><identifier>ISSN: 1054-8807</identifier><identifier>EISSN: 1879-1336</identifier><identifier>DOI: 10.1016/S1054-8807(00)00054-5</identifier><identifier>PMID: 11343989</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Animals, Inbred Strains ; Aorta, Thoracic - pathology ; Arteries ; Arteriosclerosis - blood ; Arteriosclerosis - genetics ; Arteriosclerosis - pathology ; Atherosclerosis ; Cholesterol ; Cholesterol - blood ; Disease Models, Animal ; Endothelial disruption ; Endothelium, Vascular - pathology ; Histopathology ; Hypercholesterolemia - blood ; Hypercholesterolemia - genetics ; Hypercholesterolemia - pathology ; Immunohistochemistry ; Immunostaining ; Macrophages ; Microscopy, Electron, Scanning ; Morphogenesis ; Rabbits ; Scanning electron microscopy ; Time Factors ; Transmission electron microscopy ; Tunica Intima - metabolism ; Tunica Intima - ultrastructure ; Watanabe heritable hyperlipidemic rabbit</subject><ispartof>Cardiovascular pathology, 2001-01, Vol.10 (1), p.1-11</ispartof><rights>2001 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-788133b0ef57e4a7e5bc8a9fc12483895c9990d9b703ab32c3596b887e28e533</citedby><cites>FETCH-LOGICAL-c361t-788133b0ef57e4a7e5bc8a9fc12483895c9990d9b703ab32c3596b887e28e533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S1054-8807(00)00054-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11343989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Clubb, Fred J</creatorcontrib><creatorcontrib>Cerny, Jeff L</creatorcontrib><creatorcontrib>Deferrari, Dario A</creatorcontrib><creatorcontrib>Butler-Aucoin, Michelle M</creatorcontrib><creatorcontrib>Willerson, James T</creatorcontrib><creatorcontrib>Buja, L.Maximilian</creatorcontrib><title>Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas</title><title>Cardiovascular pathology</title><addtitle>Cardiovasc Pathol</addtitle><description>To better understand the morphogenesis of atherosclerotic plaque, we evaluated temporal distribution of leukocytes, macrophages, foam cells, vascular smooth muscle cells, and subendothelial lipid in Watanabe heritable hyperlipedimic (WHHL) rabbit aortas. Aortas of WHHL (n=20) and New Zealand White (NZW, controls; n=8) rabbits were perfusion fixed at 1, 3, 6, and 12 months of age. At initial gross evaluation of lipid distribution, we identified aortic areas at high risk for lesion development. In WHHL rabbits, the lipid-positive portion of high-risk areas increased from 3% at 1 month to 50% at 12 months; during the same period, adherent cell count increased from <1 leukocyte and monocyte/mm
2 to 25 leukocytes, 44 monocytes, and 10 foam cells/mm
2. Controls showed no increase over time in lipid-positive areas or cellular adherence to the endothelium. One-month-old WHHL rabbit aortas had scattered lipid-positive cells in the intima (primarily branch points). Immunostaining of these areas did not show rabbit macrophages (RAM antibody) but were actin positive. Occasionally, platelets and monocytes adhered to the endothelial surface. By age 3 months, well-defined fatty streaks/atherosclerotic plaques had RAM-positive cells within foam cell core, along core margins, and in focal clusters in the fibrous cap and subendothelium. By age 12 months, isolated RAM-positive cells were on the endothelial surface, and surface morphology showed endothelial cell disruption foci containing clusters of macrophages and foam cells. Our results indicate that lipid accumulation (extra- and intracellular) is important in the early development of atherosclerotic lesions; a corresponding, slower accumulation of adherent cells on the lesion surface promotes lipid conversion from fatty streak to plaque.</description><subject>Animals</subject><subject>Animals, Inbred Strains</subject><subject>Aorta, Thoracic - pathology</subject><subject>Arteries</subject><subject>Arteriosclerosis - blood</subject><subject>Arteriosclerosis - genetics</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis</subject><subject>Cholesterol</subject><subject>Cholesterol - blood</subject><subject>Disease Models, Animal</subject><subject>Endothelial disruption</subject><subject>Endothelium, Vascular - pathology</subject><subject>Histopathology</subject><subject>Hypercholesterolemia - blood</subject><subject>Hypercholesterolemia - genetics</subject><subject>Hypercholesterolemia - pathology</subject><subject>Immunohistochemistry</subject><subject>Immunostaining</subject><subject>Macrophages</subject><subject>Microscopy, Electron, Scanning</subject><subject>Morphogenesis</subject><subject>Rabbits</subject><subject>Scanning electron microscopy</subject><subject>Time Factors</subject><subject>Transmission electron microscopy</subject><subject>Tunica Intima - metabolism</subject><subject>Tunica Intima - ultrastructure</subject><subject>Watanabe heritable hyperlipidemic rabbit</subject><issn>1054-8807</issn><issn>1879-1336</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEFP3DAQhS1EVSjtTwD5hOghxV7Hm_EJIWgLEhIHkHq0bGcijJw42F4Q_x4vu6hHLjNj-Xszeo-QQ85-ccaXp3ecybYBYN0JYz8ZW7_kDtnn0KmGC7HcrfMHske-5fxYIWjb9ivZ41y0QoHaJ-USnzHEecSp0DhQUx4wxexCrcU7OgfztEL64ssDxamP9Tt4E2jvc1rNxceJ-on-M8VMxiKtYl-MDXV6nTEFP_sex7onGWt9oSamYvJ38mUwIeOPbT8g939-319cNTe3f68vzm8aJ5a8NB1ANWIZDrLD1nQorQOjBscXLQhQ0imlWK9sx4SxYuGEVEsL0OECUApxQI43a-cUq4lc9OizwxDMhHGVdcdACACooNyArlrPCQc9Jz-a9Ko50-u09Xvaeh2lZky_p61l1R1tD6zsiP1_1TbeCpxtAKwunz0mnZ3HyWHvE7qi--g_OfEGp5WRdg</recordid><startdate>20010101</startdate><enddate>20010101</enddate><creator>Clubb, Fred J</creator><creator>Cerny, Jeff L</creator><creator>Deferrari, Dario A</creator><creator>Butler-Aucoin, Michelle M</creator><creator>Willerson, James T</creator><creator>Buja, L.Maximilian</creator><general>Elsevier Inc</general><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>20010101</creationdate><title>Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas</title><author>Clubb, Fred J ; Cerny, Jeff L ; Deferrari, Dario A ; Butler-Aucoin, Michelle M ; Willerson, James T ; Buja, L.Maximilian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-788133b0ef57e4a7e5bc8a9fc12483895c9990d9b703ab32c3596b887e28e533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Animals, Inbred Strains</topic><topic>Aorta, Thoracic - pathology</topic><topic>Arteries</topic><topic>Arteriosclerosis - blood</topic><topic>Arteriosclerosis - genetics</topic><topic>Arteriosclerosis - pathology</topic><topic>Atherosclerosis</topic><topic>Cholesterol</topic><topic>Cholesterol - blood</topic><topic>Disease Models, Animal</topic><topic>Endothelial disruption</topic><topic>Endothelium, Vascular - pathology</topic><topic>Histopathology</topic><topic>Hypercholesterolemia - blood</topic><topic>Hypercholesterolemia - genetics</topic><topic>Hypercholesterolemia - pathology</topic><topic>Immunohistochemistry</topic><topic>Immunostaining</topic><topic>Macrophages</topic><topic>Microscopy, Electron, Scanning</topic><topic>Morphogenesis</topic><topic>Rabbits</topic><topic>Scanning electron microscopy</topic><topic>Time Factors</topic><topic>Transmission electron microscopy</topic><topic>Tunica Intima - metabolism</topic><topic>Tunica Intima - ultrastructure</topic><topic>Watanabe heritable hyperlipidemic rabbit</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Clubb, Fred J</creatorcontrib><creatorcontrib>Cerny, Jeff L</creatorcontrib><creatorcontrib>Deferrari, Dario A</creatorcontrib><creatorcontrib>Butler-Aucoin, Michelle M</creatorcontrib><creatorcontrib>Willerson, James T</creatorcontrib><creatorcontrib>Buja, L.Maximilian</creatorcontrib><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>Cardiovascular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Clubb, Fred J</au><au>Cerny, Jeff L</au><au>Deferrari, Dario A</au><au>Butler-Aucoin, Michelle M</au><au>Willerson, James T</au><au>Buja, L.Maximilian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas</atitle><jtitle>Cardiovascular pathology</jtitle><addtitle>Cardiovasc Pathol</addtitle><date>2001-01-01</date><risdate>2001</risdate><volume>10</volume><issue>1</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>1054-8807</issn><eissn>1879-1336</eissn><abstract>To better understand the morphogenesis of atherosclerotic plaque, we evaluated temporal distribution of leukocytes, macrophages, foam cells, vascular smooth muscle cells, and subendothelial lipid in Watanabe heritable hyperlipedimic (WHHL) rabbit aortas. Aortas of WHHL (n=20) and New Zealand White (NZW, controls; n=8) rabbits were perfusion fixed at 1, 3, 6, and 12 months of age. At initial gross evaluation of lipid distribution, we identified aortic areas at high risk for lesion development. In WHHL rabbits, the lipid-positive portion of high-risk areas increased from 3% at 1 month to 50% at 12 months; during the same period, adherent cell count increased from <1 leukocyte and monocyte/mm
2 to 25 leukocytes, 44 monocytes, and 10 foam cells/mm
2. Controls showed no increase over time in lipid-positive areas or cellular adherence to the endothelium. One-month-old WHHL rabbit aortas had scattered lipid-positive cells in the intima (primarily branch points). Immunostaining of these areas did not show rabbit macrophages (RAM antibody) but were actin positive. Occasionally, platelets and monocytes adhered to the endothelial surface. By age 3 months, well-defined fatty streaks/atherosclerotic plaques had RAM-positive cells within foam cell core, along core margins, and in focal clusters in the fibrous cap and subendothelium. By age 12 months, isolated RAM-positive cells were on the endothelial surface, and surface morphology showed endothelial cell disruption foci containing clusters of macrophages and foam cells. Our results indicate that lipid accumulation (extra- and intracellular) is important in the early development of atherosclerotic lesions; a corresponding, slower accumulation of adherent cells on the lesion surface promotes lipid conversion from fatty streak to plaque.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11343989</pmid><doi>10.1016/S1054-8807(00)00054-5</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Animals, Inbred Strains Aorta, Thoracic - pathology Arteries Arteriosclerosis - blood Arteriosclerosis - genetics Arteriosclerosis - pathology Atherosclerosis Cholesterol Cholesterol - blood Disease Models, Animal Endothelial disruption Endothelium, Vascular - pathology Histopathology Hypercholesterolemia - blood Hypercholesterolemia - genetics Hypercholesterolemia - pathology Immunohistochemistry Immunostaining Macrophages Microscopy, Electron, Scanning Morphogenesis Rabbits Scanning electron microscopy Time Factors Transmission electron microscopy Tunica Intima - metabolism Tunica Intima - ultrastructure Watanabe heritable hyperlipidemic rabbit |
| title | Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas |
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