Spontaneous Elastic Tissue Lesions in the Rat Abdominal Aorta, a Genetically Determined Phenotype
In this study, phenotypic expression of spontaneous elastic laminae defects within the rat abdominal aorta was examined. Lesions in Brown Norway (BN) rats were compared with those of New Zealand genetically hypertensive (GH) rats. BN and GH rats were cross-bred to determine the phenotypic expression...
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Veröffentlicht in: | Journal of vascular research 2000-03, Vol.37 (2), p.73-81 |
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description | In this study, phenotypic expression of spontaneous elastic laminae defects within the rat abdominal aorta was examined. Lesions in Brown Norway (BN) rats were compared with those of New Zealand genetically hypertensive (GH) rats. BN and GH rats were cross-bred to determine the phenotypic expression of these lesions in successive F 1 and F 2 generations. Lesions were assessed by distribution, number and a semiquantitative index of severity. All BN aortae contained numerous elastic tissue defects. In comparison, GH aortae contained only occasional elastic tissue lesions. F 1 aortae contained lesions in numbers similar to those of the parental BN strain; however, F 1 lesions were of significantly greater severity. Within the F 2 generation, a wide range in both lesion numbers and severity indices was observed, with approximately a quarter of animals having lesion numbers analogous to the GH parental strain. In conclusion, this study indicates that the spontaneous elastic tissue lesions observed within BN rats are consistent with an autosomal dominant, possibly single gene, effect. Moreover, epistatic effects, derived from the GH strain, may influence the severity of these lesions. The gene(s) responsible may be important in the development of conditions such as arteriosclerosis and aneurysms in humans. |
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Lesions in Brown Norway (BN) rats were compared with those of New Zealand genetically hypertensive (GH) rats. BN and GH rats were cross-bred to determine the phenotypic expression of these lesions in successive F 1 and F 2 generations. Lesions were assessed by distribution, number and a semiquantitative index of severity. All BN aortae contained numerous elastic tissue defects. In comparison, GH aortae contained only occasional elastic tissue lesions. F 1 aortae contained lesions in numbers similar to those of the parental BN strain; however, F 1 lesions were of significantly greater severity. Within the F 2 generation, a wide range in both lesion numbers and severity indices was observed, with approximately a quarter of animals having lesion numbers analogous to the GH parental strain. In conclusion, this study indicates that the spontaneous elastic tissue lesions observed within BN rats are consistent with an autosomal dominant, possibly single gene, effect. Moreover, epistatic effects, derived from the GH strain, may influence the severity of these lesions. The gene(s) responsible may be important in the development of conditions such as arteriosclerosis and aneurysms in humans.</description><identifier>ISSN: 1018-1172</identifier><identifier>EISSN: 1423-0135</identifier><identifier>DOI: 10.1159/000025718</identifier><identifier>PMID: 10754392</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Animals ; Aorta, Abdominal - abnormalities ; Aorta, Abdominal - pathology ; Aorta, Abdominal - ultrastructure ; Aortic Diseases - genetics ; Aortic Diseases - pathology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Elastic Tissue - abnormalities ; Elastic Tissue - pathology ; Elastic Tissue - ultrastructure ; Female ; Male ; Medical sciences ; Phenotype ; Rats ; Rats, Inbred BN - genetics ; Rats, Inbred SHR - genetics ; Research Paper</subject><ispartof>Journal of vascular research, 2000-03, Vol.37 (2), p.73-81</ispartof><rights>2000 S. Karger AG, Basel</rights><rights>2000 INIST-CNRS</rights><rights>Copyright 2000 S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-fb02c8b61cb427e768dac6b3cccbbca113f9c50117c0e626a6ffb6c31157e9f03</citedby><cites>FETCH-LOGICAL-c388t-fb02c8b61cb427e768dac6b3cccbbca113f9c50117c0e626a6ffb6c31157e9f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1340224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10754392$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jones, Gregory T.</creatorcontrib><creatorcontrib>Harris, Eugenie L.</creatorcontrib><creatorcontrib>Jacob, Howard J.</creatorcontrib><creatorcontrib>van Rij, André M.</creatorcontrib><title>Spontaneous Elastic Tissue Lesions in the Rat Abdominal Aorta, a Genetically Determined Phenotype</title><title>Journal of vascular research</title><addtitle>J Vasc Res</addtitle><description>In this study, phenotypic expression of spontaneous elastic laminae defects within the rat abdominal aorta was examined. Lesions in Brown Norway (BN) rats were compared with those of New Zealand genetically hypertensive (GH) rats. BN and GH rats were cross-bred to determine the phenotypic expression of these lesions in successive F 1 and F 2 generations. Lesions were assessed by distribution, number and a semiquantitative index of severity. All BN aortae contained numerous elastic tissue defects. In comparison, GH aortae contained only occasional elastic tissue lesions. F 1 aortae contained lesions in numbers similar to those of the parental BN strain; however, F 1 lesions were of significantly greater severity. Within the F 2 generation, a wide range in both lesion numbers and severity indices was observed, with approximately a quarter of animals having lesion numbers analogous to the GH parental strain. In conclusion, this study indicates that the spontaneous elastic tissue lesions observed within BN rats are consistent with an autosomal dominant, possibly single gene, effect. Moreover, epistatic effects, derived from the GH strain, may influence the severity of these lesions. The gene(s) responsible may be important in the development of conditions such as arteriosclerosis and aneurysms in humans.</description><subject>Animals</subject><subject>Aorta, Abdominal - abnormalities</subject><subject>Aorta, Abdominal - pathology</subject><subject>Aorta, Abdominal - ultrastructure</subject><subject>Aortic Diseases - genetics</subject><subject>Aortic Diseases - pathology</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>Elastic Tissue - abnormalities</subject><subject>Elastic Tissue - pathology</subject><subject>Elastic Tissue - ultrastructure</subject><subject>Female</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Phenotype</subject><subject>Rats</subject><subject>Rats, Inbred BN - genetics</subject><subject>Rats, Inbred SHR - genetics</subject><subject>Research Paper</subject><issn>1018-1172</issn><issn>1423-0135</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0MtLJDEQB-AgirrqwbMgQZYFwdZU0o_0cXB9MqD4ujZJurL22tPdm2QO899vtEfXw4K5JFBfqqgfIbvAjgGy8oTFw7MC5ArZhJSLhIHIVuObgUwACr5Bvnn_mzFIS5mvkw1gRZaKkm8SdT_0XVAd9nNPz1rlQ2PoQ-P9HOkUfdN3njYdDc9I71SgE133s6ZTLZ30LqgjqugFdhg_qbZd0J8Y0MU61vT2Gbs-LAbcJmtWtR53lvcWeTw_ezi9TKY3F1enk2lihJQhsZpxI3UORqe8wCKXtTK5FsYYrY0CELY0GYvbGIY5z1Vurc6NiAEUWFomtsiPse_g-j9z9KGaNd5g247LVQUwXmYSvoQcuChlVkZ4OELjeu8d2mpwzUy5RQWseg2--gg-2v1l07meYf1JjklH8H0JlI9hWac60_h_TqSM8zSyvZG9KPcL3Uf9fcrBf6vXT3dvoBpqK_4CDfSe8g</recordid><startdate>20000301</startdate><enddate>20000301</enddate><creator>Jones, Gregory T.</creator><creator>Harris, Eugenie L.</creator><creator>Jacob, Howard J.</creator><creator>van Rij, André M.</creator><general>Karger</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20000301</creationdate><title>Spontaneous Elastic Tissue Lesions in the Rat Abdominal Aorta, a Genetically Determined Phenotype</title><author>Jones, Gregory T. ; Harris, Eugenie L. ; Jacob, Howard J. ; van Rij, André M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-fb02c8b61cb427e768dac6b3cccbbca113f9c50117c0e626a6ffb6c31157e9f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Aorta, Abdominal - abnormalities</topic><topic>Aorta, Abdominal - pathology</topic><topic>Aorta, Abdominal - ultrastructure</topic><topic>Aortic Diseases - genetics</topic><topic>Aortic Diseases - pathology</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>Elastic Tissue - abnormalities</topic><topic>Elastic Tissue - pathology</topic><topic>Elastic Tissue - ultrastructure</topic><topic>Female</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Phenotype</topic><topic>Rats</topic><topic>Rats, Inbred BN - genetics</topic><topic>Rats, Inbred SHR - genetics</topic><topic>Research Paper</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jones, Gregory T.</creatorcontrib><creatorcontrib>Harris, Eugenie L.</creatorcontrib><creatorcontrib>Jacob, Howard J.</creatorcontrib><creatorcontrib>van Rij, André 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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of vascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jones, Gregory T.</au><au>Harris, Eugenie L.</au><au>Jacob, Howard J.</au><au>van Rij, André M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spontaneous Elastic Tissue Lesions in the Rat Abdominal Aorta, a Genetically Determined Phenotype</atitle><jtitle>Journal of vascular research</jtitle><addtitle>J Vasc Res</addtitle><date>2000-03-01</date><risdate>2000</risdate><volume>37</volume><issue>2</issue><spage>73</spage><epage>81</epage><pages>73-81</pages><issn>1018-1172</issn><eissn>1423-0135</eissn><abstract>In this study, phenotypic expression of spontaneous elastic laminae defects within the rat abdominal aorta was examined. Lesions in Brown Norway (BN) rats were compared with those of New Zealand genetically hypertensive (GH) rats. BN and GH rats were cross-bred to determine the phenotypic expression of these lesions in successive F 1 and F 2 generations. Lesions were assessed by distribution, number and a semiquantitative index of severity. All BN aortae contained numerous elastic tissue defects. In comparison, GH aortae contained only occasional elastic tissue lesions. F 1 aortae contained lesions in numbers similar to those of the parental BN strain; however, F 1 lesions were of significantly greater severity. Within the F 2 generation, a wide range in both lesion numbers and severity indices was observed, with approximately a quarter of animals having lesion numbers analogous to the GH parental strain. In conclusion, this study indicates that the spontaneous elastic tissue lesions observed within BN rats are consistent with an autosomal dominant, possibly single gene, effect. Moreover, epistatic effects, derived from the GH strain, may influence the severity of these lesions. The gene(s) responsible may be important in the development of conditions such as arteriosclerosis and aneurysms in humans.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>10754392</pmid><doi>10.1159/000025718</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Aorta, Abdominal - abnormalities Aorta, Abdominal - pathology Aorta, Abdominal - ultrastructure Aortic Diseases - genetics Aortic Diseases - pathology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Elastic Tissue - abnormalities Elastic Tissue - pathology Elastic Tissue - ultrastructure Female Male Medical sciences Phenotype Rats Rats, Inbred BN - genetics Rats, Inbred SHR - genetics Research Paper |
title | Spontaneous Elastic Tissue Lesions in the Rat Abdominal Aorta, a Genetically Determined Phenotype |
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