Divergence of beta-myosin heavy chain (betaMHC) expression in fetal rat cardiomyocytes in vitro and adult rat heart in vivo
The myosin heavy chain gene products are an important determinant of myocardial functional properties. Although a strong positive element (beta f1) within the betaMHC promoter region has previously been identified, to date no species comparisons in promoter strength have been made. To examine this q...
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Veröffentlicht in: | Biochemical and biophysical research communications 1997-01, Vol.230 (2), p.340-343 |
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description | The myosin heavy chain gene products are an important determinant of myocardial functional properties. Although a strong positive element (beta f1) within the betaMHC promoter region has previously been identified, to date no species comparisons in promoter strength have been made. To examine this question, we have used betaMHC deletion constructs, containing the rat or human beta f1 enhancer region, to determine expression both in vitro using rat fetal cardiomyocytes and in vivo by direct injection into adult rat heart. When reporter constructs were transfected into cultured fetal rat cardiomyocytes, the human beta reporter was expressed more than 3 fold above the equivalent rat construct. Exchange of the beta f1 enhancer indicated that the human sequence of the beta f1 enhancer was largely responsible. However, these findings were not replicated when the reporters were injected into the adult rat heart. In the adult myocardium the levels of reporter expression were similar for the betaMHC promoter reporters studied. These findings demonstrate a divergence between primary cardiomyocytes maintained in culture and the cardiomyocytes found within the intact adult heart. |
doi_str_mv | 10.1006/bbrc.1996.5963 |
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Although a strong positive element (beta f1) within the betaMHC promoter region has previously been identified, to date no species comparisons in promoter strength have been made. To examine this question, we have used betaMHC deletion constructs, containing the rat or human beta f1 enhancer region, to determine expression both in vitro using rat fetal cardiomyocytes and in vivo by direct injection into adult rat heart. When reporter constructs were transfected into cultured fetal rat cardiomyocytes, the human beta reporter was expressed more than 3 fold above the equivalent rat construct. Exchange of the beta f1 enhancer indicated that the human sequence of the beta f1 enhancer was largely responsible. However, these findings were not replicated when the reporters were injected into the adult rat heart. In the adult myocardium the levels of reporter expression were similar for the betaMHC promoter reporters studied. 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Although a strong positive element (beta f1) within the betaMHC promoter region has previously been identified, to date no species comparisons in promoter strength have been made. To examine this question, we have used betaMHC deletion constructs, containing the rat or human beta f1 enhancer region, to determine expression both in vitro using rat fetal cardiomyocytes and in vivo by direct injection into adult rat heart. When reporter constructs were transfected into cultured fetal rat cardiomyocytes, the human beta reporter was expressed more than 3 fold above the equivalent rat construct. Exchange of the beta f1 enhancer indicated that the human sequence of the beta f1 enhancer was largely responsible. However, these findings were not replicated when the reporters were injected into the adult rat heart. In the adult myocardium the levels of reporter expression were similar for the betaMHC promoter reporters studied. These findings demonstrate a divergence between primary cardiomyocytes maintained in culture and the cardiomyocytes found within the intact adult heart.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Cells, Cultured</subject><subject>Enhancer Elements, Genetic</subject><subject>Fetal Heart - metabolism</subject><subject>Gene Deletion</subject><subject>Humans</subject><subject>Myocardium - metabolism</subject><subject>Myosin Heavy Chains - biosynthesis</subject><subject>Myosin Heavy Chains - genetics</subject><subject>Rabbits</subject><subject>Rats</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>Swine</subject><subject>Transfection</subject><issn>0006-291X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotkL1PwzAQxT2ASimsbEieEAwpduI49ojKR5GKWEBii2znQoPyhe1ERPzzuLTTnX7v3ZPeIXRByZISwm-1tmZJpeTLVPLkCM1JoFEs6ccJOnXuixBKGZczNJOE8iyTc_R7X41gP6E1gLsSa_AqaqbOVS3eghonbLYq7Nc74WW9usHw01twrupaHHgZcI2t8tgoW1RdODWTB7fTxsrbDqu2wKoYav_vCpnW78WxO0PHpaodnB_mAr0_Pryt1tHm9el5dbeJ-phwHwmd6FJkVGgwJE5lygpGpDRMai04hZhBYQSjXMSMpoxwlsYiVM1SlRCuIFmgq31ub7vvAZzPm8oZqGvVQje4PBOZlDTjwXh5MA66gSLvbdUoO-WHbyV_DAhqkQ</recordid><startdate>19970113</startdate><enddate>19970113</enddate><creator>Edwards, J G</creator><creator>Ghaleh, B</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19970113</creationdate><title>Divergence of beta-myosin heavy chain (betaMHC) expression in fetal rat cardiomyocytes in vitro and adult rat heart in vivo</title><author>Edwards, J G ; Ghaleh, B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p206t-8b3bf8718bec025954d4099c49bb861e24edc841682415406452800175a306ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Cells, Cultured</topic><topic>Enhancer Elements, Genetic</topic><topic>Fetal Heart - metabolism</topic><topic>Gene Deletion</topic><topic>Humans</topic><topic>Myocardium - metabolism</topic><topic>Myosin Heavy Chains - biosynthesis</topic><topic>Myosin Heavy Chains - genetics</topic><topic>Rabbits</topic><topic>Rats</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>Swine</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Edwards, J G</creatorcontrib><creatorcontrib>Ghaleh, B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Edwards, J G</au><au>Ghaleh, B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Divergence of beta-myosin heavy chain (betaMHC) expression in fetal rat cardiomyocytes in vitro and adult rat heart in vivo</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1997-01-13</date><risdate>1997</risdate><volume>230</volume><issue>2</issue><spage>340</spage><epage>343</epage><pages>340-343</pages><issn>0006-291X</issn><abstract>The myosin heavy chain gene products are an important determinant of myocardial functional properties. Although a strong positive element (beta f1) within the betaMHC promoter region has previously been identified, to date no species comparisons in promoter strength have been made. To examine this question, we have used betaMHC deletion constructs, containing the rat or human beta f1 enhancer region, to determine expression both in vitro using rat fetal cardiomyocytes and in vivo by direct injection into adult rat heart. When reporter constructs were transfected into cultured fetal rat cardiomyocytes, the human beta reporter was expressed more than 3 fold above the equivalent rat construct. Exchange of the beta f1 enhancer indicated that the human sequence of the beta f1 enhancer was largely responsible. However, these findings were not replicated when the reporters were injected into the adult rat heart. In the adult myocardium the levels of reporter expression were similar for the betaMHC promoter reporters studied. These findings demonstrate a divergence between primary cardiomyocytes maintained in culture and the cardiomyocytes found within the intact adult heart.</abstract><cop>United States</cop><pmid>9016779</pmid><doi>10.1006/bbrc.1996.5963</doi><tpages>4</tpages></addata></record> |
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subjects | Animals Base Sequence Cells, Cultured Enhancer Elements, Genetic Fetal Heart - metabolism Gene Deletion Humans Myocardium - metabolism Myosin Heavy Chains - biosynthesis Myosin Heavy Chains - genetics Rabbits Rats Recombinant Proteins - biosynthesis Swine Transfection |
title | Divergence of beta-myosin heavy chain (betaMHC) expression in fetal rat cardiomyocytes in vitro and adult rat heart in vivo |
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