B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury
OBJECTIVES—The function of B-Myb, a negative regulator of vascular smooth muscle cell (SMC) matrix gene transcription, was analyzed in the vasculature. METHODS AND RESULTS—Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identifi...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-09, Vol.24 (9), p.1608-1613 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Hofmann, Claudia S Sullivan, Christopher P Jiang, Hao-Yuan Stone, Phillip J Toselli, Paul Reis, Ernane D Chereshnev, Igor Schreiber, Barbara M Sonenshein, Gail E |
| description | OBJECTIVES—The function of B-Myb, a negative regulator of vascular smooth muscle cell (SMC) matrix gene transcription, was analyzed in the vasculature.
METHODS AND RESULTS—Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identified. Mice appeared to develop normally, and human B-myb was expressed in the aortas. Total B-Myb levels were elevated in aortas of adult transgenic versus wild-type (WT) animals and varied inversely with α1(I) collagen mRNA expression. However, neonatal WT and transgenic aortas displayed comparable levels of α1(I) collagen mRNA, likely resulting from elevated levels of cyclin A, which ablated repression by B-Myb. Aortic SMCs from adult transgenic animals displayed decreased α1(I) collagen mRNA levels. To examine the role of B-Myb after vascular injury, animals were subjected to femoral artery denudation, which induces SMC-rich lesion formation. A dramatic reduction in neointima formation and lumenal narrowing was observed in arteries of B-myb transgenic versus WT mice 4 weeks after injury.
CONCLUSIONS—Data indicate that B-Myb, which inhibits matrix gene expression in the adult vessel wall, reduces neointima formation after vascular injury. |
| doi_str_mv | 10.1161/01.ATV.0000139010.71779.f3 |
| format | Article |
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METHODS AND RESULTS—Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identified. Mice appeared to develop normally, and human B-myb was expressed in the aortas. Total B-Myb levels were elevated in aortas of adult transgenic versus wild-type (WT) animals and varied inversely with α1(I) collagen mRNA expression. However, neonatal WT and transgenic aortas displayed comparable levels of α1(I) collagen mRNA, likely resulting from elevated levels of cyclin A, which ablated repression by B-Myb. Aortic SMCs from adult transgenic animals displayed decreased α1(I) collagen mRNA levels. To examine the role of B-Myb after vascular injury, animals were subjected to femoral artery denudation, which induces SMC-rich lesion formation. A dramatic reduction in neointima formation and lumenal narrowing was observed in arteries of B-myb transgenic versus WT mice 4 weeks after injury.
CONCLUSIONS—Data indicate that B-Myb, which inhibits matrix gene expression in the adult vessel wall, reduces neointima formation after vascular injury.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000139010.71779.f3</identifier><identifier>PMID: 15256398</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Age Factors ; Animals ; Animals, Newborn ; Aorta - metabolism ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Cycle Proteins - biosynthesis ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - physiology ; Collagen - biosynthesis ; Collagen - genetics ; Cyclin A - biosynthesis ; Cyclin A - genetics ; Cytomegalovirus - genetics ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; DNA-Binding Proteins - biosynthesis ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - physiology ; Female ; Femoral Artery - injuries ; Femoral Artery - metabolism ; Femoral Artery - pathology ; Gene Expression Regulation ; Human cytomegalovirus ; Humans ; Male ; Medical sciences ; Mice ; Mice, Transgenic ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; Promoter Regions, Genetic ; RNA, Messenger - biosynthesis ; Trans-Activators - biosynthesis ; Trans-Activators - genetics ; Trans-Activators - physiology ; Transgenes ; Tunica Intima - pathology</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-09, Vol.24 (9), p.1608-1613</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5072-adccd5898bf473e8bbd36bcceb27987578cf38adffa5a672621cd2da54ed757b3</citedby><cites>FETCH-LOGICAL-c5072-adccd5898bf473e8bbd36bcceb27987578cf38adffa5a672621cd2da54ed757b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16097556$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15256398$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hofmann, Claudia S</creatorcontrib><creatorcontrib>Sullivan, Christopher P</creatorcontrib><creatorcontrib>Jiang, Hao-Yuan</creatorcontrib><creatorcontrib>Stone, Phillip J</creatorcontrib><creatorcontrib>Toselli, Paul</creatorcontrib><creatorcontrib>Reis, Ernane D</creatorcontrib><creatorcontrib>Chereshnev, Igor</creatorcontrib><creatorcontrib>Schreiber, Barbara M</creatorcontrib><creatorcontrib>Sonenshein, Gail E</creatorcontrib><title>B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVES—The function of B-Myb, a negative regulator of vascular smooth muscle cell (SMC) matrix gene transcription, was analyzed in the vasculature.
METHODS AND RESULTS—Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identified. Mice appeared to develop normally, and human B-myb was expressed in the aortas. Total B-Myb levels were elevated in aortas of adult transgenic versus wild-type (WT) animals and varied inversely with α1(I) collagen mRNA expression. However, neonatal WT and transgenic aortas displayed comparable levels of α1(I) collagen mRNA, likely resulting from elevated levels of cyclin A, which ablated repression by B-Myb. Aortic SMCs from adult transgenic animals displayed decreased α1(I) collagen mRNA levels. To examine the role of B-Myb after vascular injury, animals were subjected to femoral artery denudation, which induces SMC-rich lesion formation. A dramatic reduction in neointima formation and lumenal narrowing was observed in arteries of B-myb transgenic versus WT mice 4 weeks after injury.
CONCLUSIONS—Data indicate that B-Myb, which inhibits matrix gene expression in the adult vessel wall, reduces neointima formation after vascular injury.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Aorta - metabolism</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>Cell Cycle Proteins - biosynthesis</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - physiology</subject><subject>Collagen - biosynthesis</subject><subject>Collagen - genetics</subject><subject>Cyclin A - biosynthesis</subject><subject>Cyclin A - genetics</subject><subject>Cytomegalovirus - genetics</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Female</subject><subject>Femoral Artery - injuries</subject><subject>Femoral Artery - metabolism</subject><subject>Femoral Artery - pathology</subject><subject>Gene Expression Regulation</subject><subject>Human cytomegalovirus</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>Promoter Regions, Genetic</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Trans-Activators - biosynthesis</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - physiology</subject><subject>Transgenes</subject><subject>Tunica Intima - pathology</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1vEzEQhi0EoiXwF5CFBLcN_lh_cQtRWyq1IEHp1fJ6Z8kWZ53auypR_3ydJlKO-GCP7eed8fhF6AMlc0ol_UzofHFzOydlUG5IOVZUKTPv-At0SgWrq1py-bLERJlKyJqdoDc53xW-Zoy8RicFEpIbfYoev1bX2wb_hE2CnCHjW5f9FFzCv9Yxjit8PWUfAC8hBLyMIbg_MOALGACf_XvW9HHAbmjx5bDqm37M-DvEfhj7tcPnMa3duAMW3QgJL1KZexcKezel7Vv0qnMhw7vDOkO_z89ult-qqx8Xl8vFVeUFUaxyrfet0EY3Xa046KZpuWy8h4Ypo5VQ2ndcu7brnHBSMcmob1nrRA1tuW34DH3a592keD9BHu26z7405AaIU7ZS6pooof8LUmOYVtIU8Mse9CnmnKCzm1QaTltLid15ZAm1xSN79Mg-e2Q7XsTvD1WmZg3tUXowpQAfD0DxwoUuucH3-chJYpQo6AzVe-4hhvKx-W-YHiDZFbgwrnalay6JqFgJiCnbavcYxp8AyeWsLA</recordid><startdate>200409</startdate><enddate>200409</enddate><creator>Hofmann, Claudia S</creator><creator>Sullivan, Christopher P</creator><creator>Jiang, Hao-Yuan</creator><creator>Stone, Phillip J</creator><creator>Toselli, Paul</creator><creator>Reis, Ernane D</creator><creator>Chereshnev, Igor</creator><creator>Schreiber, Barbara M</creator><creator>Sonenshein, Gail E</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>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200409</creationdate><title>B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury</title><author>Hofmann, Claudia S ; Sullivan, Christopher P ; Jiang, Hao-Yuan ; Stone, Phillip J ; Toselli, Paul ; Reis, Ernane D ; Chereshnev, Igor ; Schreiber, Barbara M ; Sonenshein, Gail E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5072-adccd5898bf473e8bbd36bcceb27987578cf38adffa5a672621cd2da54ed757b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Aorta - metabolism</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>Cell Cycle Proteins - biosynthesis</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - physiology</topic><topic>Collagen - biosynthesis</topic><topic>Collagen - genetics</topic><topic>Cyclin A - biosynthesis</topic><topic>Cyclin A - genetics</topic><topic>Cytomegalovirus - genetics</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Female</topic><topic>Femoral Artery - injuries</topic><topic>Femoral Artery - metabolism</topic><topic>Femoral Artery - pathology</topic><topic>Gene Expression Regulation</topic><topic>Human cytomegalovirus</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Myocytes, Smooth Muscle - pathology</topic><topic>Promoter Regions, Genetic</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Trans-Activators - biosynthesis</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - physiology</topic><topic>Transgenes</topic><topic>Tunica Intima - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hofmann, Claudia S</creatorcontrib><creatorcontrib>Sullivan, Christopher P</creatorcontrib><creatorcontrib>Jiang, Hao-Yuan</creatorcontrib><creatorcontrib>Stone, Phillip J</creatorcontrib><creatorcontrib>Toselli, Paul</creatorcontrib><creatorcontrib>Reis, Ernane D</creatorcontrib><creatorcontrib>Chereshnev, Igor</creatorcontrib><creatorcontrib>Schreiber, Barbara M</creatorcontrib><creatorcontrib>Sonenshein, Gail E</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>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</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>Hofmann, Claudia S</au><au>Sullivan, Christopher P</au><au>Jiang, Hao-Yuan</au><au>Stone, Phillip J</au><au>Toselli, Paul</au><au>Reis, Ernane D</au><au>Chereshnev, Igor</au><au>Schreiber, Barbara M</au><au>Sonenshein, Gail E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-09</date><risdate>2004</risdate><volume>24</volume><issue>9</issue><spage>1608</spage><epage>1613</epage><pages>1608-1613</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVES—The function of B-Myb, a negative regulator of vascular smooth muscle cell (SMC) matrix gene transcription, was analyzed in the vasculature.
METHODS AND RESULTS—Mice were generated in which the human B-myb gene was driven by the basal cytomegalovirus promoter, and 3 founders were identified. Mice appeared to develop normally, and human B-myb was expressed in the aortas. Total B-Myb levels were elevated in aortas of adult transgenic versus wild-type (WT) animals and varied inversely with α1(I) collagen mRNA expression. However, neonatal WT and transgenic aortas displayed comparable levels of α1(I) collagen mRNA, likely resulting from elevated levels of cyclin A, which ablated repression by B-Myb. Aortic SMCs from adult transgenic animals displayed decreased α1(I) collagen mRNA levels. To examine the role of B-Myb after vascular injury, animals were subjected to femoral artery denudation, which induces SMC-rich lesion formation. A dramatic reduction in neointima formation and lumenal narrowing was observed in arteries of B-myb transgenic versus WT mice 4 weeks after injury.
CONCLUSIONS—Data indicate that B-Myb, which inhibits matrix gene expression in the adult vessel wall, reduces neointima formation after vascular injury.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15256398</pmid><doi>10.1161/01.ATV.0000139010.71779.f3</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2004-09, Vol.24 (9), p.1608-1613 |
| issn | 1079-5642 1524-4636 |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Age Factors Animals Animals, Newborn Aorta - metabolism Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Cycle Proteins - biosynthesis Cell Cycle Proteins - genetics Cell Cycle Proteins - physiology Collagen - biosynthesis Collagen - genetics Cyclin A - biosynthesis Cyclin A - genetics Cytomegalovirus - genetics Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous DNA-Binding Proteins - biosynthesis DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Female Femoral Artery - injuries Femoral Artery - metabolism Femoral Artery - pathology Gene Expression Regulation Human cytomegalovirus Humans Male Medical sciences Mice Mice, Transgenic Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology Promoter Regions, Genetic RNA, Messenger - biosynthesis Trans-Activators - biosynthesis Trans-Activators - genetics Trans-Activators - physiology Transgenes Tunica Intima - pathology |
| title | B-Myb Represses Vascular Smooth Muscle Cell Collagen Gene Expression and Inhibits Neointima Formation After Arterial Injury |
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