Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload–Induced Cardiac Hypertrophy
Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC)...
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Veröffentlicht in: | Circulation research 2008-12, Vol.103 (12), p.1359-1362 |
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creator | Mitchell-Jordan, Scherise A Holopainen, Tanja Ren, Shuxun Wang, Sujing Warburton, Sarah Zhang, Michael J Alitalo, Kari Wang, Yibin Vondriska, Thomas M |
description | Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload–induced hypertrophic growth. |
doi_str_mv | 10.1161/CIRCRESAHA.108.186577 |
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To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload–induced hypertrophic growth.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.108.186577</identifier><identifier>PMID: 18988895</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - genetics ; Blood Pressure - physiology ; Cardiomegaly - genetics ; Cardiomegaly - metabolism ; Cardiomegaly - prevention & control ; Fundamental and applied biological sciences. Psychology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Protein-Tyrosine Kinases - deficiency ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - physiology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2008-12, Vol.103 (12), p.1359-1362</ispartof><rights>2008 American Heart Association, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4685-f8332a23c60c6f9096a7268e6d108736666fd9f23872ddf61fa83d2fe7dc73513</citedby><cites>FETCH-LOGICAL-c4685-f8332a23c60c6f9096a7268e6d108736666fd9f23872ddf61fa83d2fe7dc73513</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=20942413$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18988895$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mitchell-Jordan, Scherise A</creatorcontrib><creatorcontrib>Holopainen, Tanja</creatorcontrib><creatorcontrib>Ren, Shuxun</creatorcontrib><creatorcontrib>Wang, Sujing</creatorcontrib><creatorcontrib>Warburton, Sarah</creatorcontrib><creatorcontrib>Zhang, Michael J</creatorcontrib><creatorcontrib>Alitalo, Kari</creatorcontrib><creatorcontrib>Wang, Yibin</creatorcontrib><creatorcontrib>Vondriska, Thomas M</creatorcontrib><title>Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload–Induced Cardiac Hypertrophy</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload–induced hypertrophic growth.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - genetics</subject><subject>Blood Pressure - physiology</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - prevention & control</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Protein-Tyrosine Kinases - deficiency</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Protein-Tyrosine Kinases - physiology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkc1uEzEQxy0EomnhEUC-0NsGf6w_9hhWLYkaUVTK2Rh7rCxs1lt7tyW3vgNvyJN0o0R0LjP66zczmv8g9I6SOaWSfqxXN_XNxbfFcjGnRM-plkKpF2hGBSuLUij6Es0IIVWhOCcn6DTnX4TQkrPqNTqhutJaV2KGfqxjzjgG_Gn7B3-JXQIH_RATvt2lmJsO8FXT2Qz4a4J76Ia8L3IeE-Dre0httP7f499V50cHHtc2-cY6vNz1kIYU-83uDXoVbJvh7TGfoe-XF7f1slhff17Vi3XhSqlFETTnzDLuJHEyVKSSVjGpQfrpOsXlFMFXgXGtmPdB0mA19yyA8k5xQfkZOj_M7VO8GyEPZttkB21rO4hjNrLSSijJJlAcQDcdmBME06dma9POUGL21ppnaydJm4O1U9_744Lx5xb8c9fRywn4cARsdrYNyXauyf85RqqSlZRPXHngHmI7QMq_2_EBktmAbYeNmX5GOKGsYIRoyoggxV4S_Al20JNo</recordid><startdate>20081205</startdate><enddate>20081205</enddate><creator>Mitchell-Jordan, Scherise A</creator><creator>Holopainen, Tanja</creator><creator>Ren, Shuxun</creator><creator>Wang, Sujing</creator><creator>Warburton, Sarah</creator><creator>Zhang, Michael J</creator><creator>Alitalo, Kari</creator><creator>Wang, Yibin</creator><creator>Vondriska, Thomas M</creator><general>American Heart Association, Inc</general><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>20081205</creationdate><title>Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload–Induced Cardiac Hypertrophy</title><author>Mitchell-Jordan, Scherise A ; Holopainen, Tanja ; Ren, Shuxun ; Wang, Sujing ; Warburton, Sarah ; Zhang, Michael J ; Alitalo, Kari ; Wang, Yibin ; Vondriska, Thomas M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4685-f8332a23c60c6f9096a7268e6d108736666fd9f23872ddf61fa83d2fe7dc73513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - genetics</topic><topic>Blood Pressure - physiology</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomegaly - prevention & control</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Protein-Tyrosine Kinases - deficiency</topic><topic>Protein-Tyrosine Kinases - genetics</topic><topic>Protein-Tyrosine Kinases - physiology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mitchell-Jordan, Scherise A</creatorcontrib><creatorcontrib>Holopainen, Tanja</creatorcontrib><creatorcontrib>Ren, Shuxun</creatorcontrib><creatorcontrib>Wang, Sujing</creatorcontrib><creatorcontrib>Warburton, Sarah</creatorcontrib><creatorcontrib>Zhang, Michael J</creatorcontrib><creatorcontrib>Alitalo, Kari</creatorcontrib><creatorcontrib>Wang, Yibin</creatorcontrib><creatorcontrib>Vondriska, Thomas 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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mitchell-Jordan, Scherise A</au><au>Holopainen, Tanja</au><au>Ren, Shuxun</au><au>Wang, Sujing</au><au>Warburton, Sarah</au><au>Zhang, Michael J</au><au>Alitalo, Kari</au><au>Wang, Yibin</au><au>Vondriska, Thomas M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload–Induced Cardiac Hypertrophy</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2008-12-05</date><risdate>2008</risdate><volume>103</volume><issue>12</issue><spage>1359</spage><epage>1362</epage><pages>1359-1362</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload–induced hypertrophic growth.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>18988895</pmid><doi>10.1161/CIRCRESAHA.108.186577</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Blood Pressure - genetics Blood Pressure - physiology Cardiomegaly - genetics Cardiomegaly - metabolism Cardiomegaly - prevention & control Fundamental and applied biological sciences. Psychology Male Mice Mice, Inbred BALB C Mice, Knockout Protein-Tyrosine Kinases - deficiency Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - physiology Vertebrates: cardiovascular system |
title | Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload–Induced Cardiac Hypertrophy |
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