Expression of Proto-oncogenes and Gene Mutation of Sarcomeric Proteins in Patients With Hypertrophic Cardiomyopathy
Several mutations of cardiac beta-myosin heavy chain (beta-MHC) gene were reported in patients with hypertrophic cardiomyopathy (HCM). Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc exp...
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| Veröffentlicht in: | Circulation research 1998-09, Vol.83 (6), p.594-601 |
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| creator | Kai, Hisashi Muraishi, Akihiko Sugiu, Yuji Nishi, Hirohumi Seki, Yukihiko Kuwahara, Fumitaka Kimura, Akinori Kato, Hirohisa Imaizumi, Tsutomu |
| description | Several mutations of cardiac beta-myosin heavy chain (beta-MHC) gene were reported in patients with hypertrophic cardiomyopathy (HCM). Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc expression in the steady-state myocardium on hypertrophic changes and to evaluate the possible interaction between beta-MHC mutation and proto-oncogene expression in HCM. Endomyocardial biopsy was performed in 17 HCM patients (5 beta-MHC mutations and 1 troponin T mutation) and 7 control subjects (no mutation). Reverse transcription-polymerase chain reaction analysis revealed c-H-ras expression in all members of both groups. Cardiomyocyte size was correlated with the expression level of c-H-ras (P |
| doi_str_mv | 10.1161/01.RES.83.6.594 |
| format | Article |
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Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc expression in the steady-state myocardium on hypertrophic changes and to evaluate the possible interaction between beta-MHC mutation and proto-oncogene expression in HCM. Endomyocardial biopsy was performed in 17 HCM patients (5 beta-MHC mutations and 1 troponin T mutation) and 7 control subjects (no mutation). Reverse transcription-polymerase chain reaction analysis revealed c-H-ras expression in all members of both groups. Cardiomyocyte size was correlated with the expression level of c-H-ras (P<0.001), and c-H-ras expression was upregulated in HCM patients (P<0.01). HCM patients with a beta-MHC mutation had the higher c-H-ras expression than did control subjects or patients without a mutation (P<0.01). c-myc mRNA was expressed in 7 of 17 HCM patients but not in control subjects. Myocyte size was greater in c-myc-positive HCM patients than in control subjects and c-myc-negative HCM patients (P<0.001 and P<0.05, respectively). The proto-oncogene expression did not affect clinical findings, myocardial fibrosis, or disarray. In conclusion, c-H-ras and c-myc expression in the steady-state myocardium may play a role in the hypertrophic mechanism in HCM. It is possible that beta-MHC gene mutation has some effect on the regulation of proto-oncogene expression in HCM. (Circ Res. 1998;83:594-601.)</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.83.6.594</identifier><identifier>PMID: 9742054</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Adolescent ; Adult ; Aged ; Biological and medical sciences ; Biopsy ; Cardiology. Vascular system ; Cardiomyopathy, Hypertrophic - genetics ; Female ; Gene Expression ; Genes, MHC Class II - genetics ; Genes, ras - genetics ; Heart ; Humans ; Male ; Medical sciences ; Middle Aged ; Muscle Proteins - genetics ; Mutation ; Myocarditis. Cardiomyopathies ; Myocardium - metabolism ; Myocardium - pathology ; Polymerase Chain Reaction ; Proto-Oncogenes - genetics ; RNA, Messenger - genetics ; RNA-Directed DNA Polymerase ; Sarcomeres - chemistry</subject><ispartof>Circulation research, 1998-09, Vol.83 (6), p.594-601</ispartof><rights>1998 American Heart Association, Inc.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Sep 21, 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4703-27df15c7ec7e99c87da2fd50228baa2b04ee391763eb35300d20cf2575a11d803</citedby><cites>FETCH-LOGICAL-c4703-27df15c7ec7e99c87da2fd50228baa2b04ee391763eb35300d20cf2575a11d803</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3686,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2402607$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9742054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kai, Hisashi</creatorcontrib><creatorcontrib>Muraishi, Akihiko</creatorcontrib><creatorcontrib>Sugiu, Yuji</creatorcontrib><creatorcontrib>Nishi, Hirohumi</creatorcontrib><creatorcontrib>Seki, Yukihiko</creatorcontrib><creatorcontrib>Kuwahara, Fumitaka</creatorcontrib><creatorcontrib>Kimura, Akinori</creatorcontrib><creatorcontrib>Kato, Hirohisa</creatorcontrib><creatorcontrib>Imaizumi, Tsutomu</creatorcontrib><title>Expression of Proto-oncogenes and Gene Mutation of Sarcomeric Proteins in Patients With Hypertrophic Cardiomyopathy</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Several mutations of cardiac beta-myosin heavy chain (beta-MHC) gene were reported in patients with hypertrophic cardiomyopathy (HCM). Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc expression in the steady-state myocardium on hypertrophic changes and to evaluate the possible interaction between beta-MHC mutation and proto-oncogene expression in HCM. Endomyocardial biopsy was performed in 17 HCM patients (5 beta-MHC mutations and 1 troponin T mutation) and 7 control subjects (no mutation). Reverse transcription-polymerase chain reaction analysis revealed c-H-ras expression in all members of both groups. Cardiomyocyte size was correlated with the expression level of c-H-ras (P<0.001), and c-H-ras expression was upregulated in HCM patients (P<0.01). HCM patients with a beta-MHC mutation had the higher c-H-ras expression than did control subjects or patients without a mutation (P<0.01). c-myc mRNA was expressed in 7 of 17 HCM patients but not in control subjects. Myocyte size was greater in c-myc-positive HCM patients than in control subjects and c-myc-negative HCM patients (P<0.001 and P<0.05, respectively). The proto-oncogene expression did not affect clinical findings, myocardial fibrosis, or disarray. In conclusion, c-H-ras and c-myc expression in the steady-state myocardium may play a role in the hypertrophic mechanism in HCM. It is possible that beta-MHC gene mutation has some effect on the regulation of proto-oncogene expression in HCM. (Circ Res. 1998;83:594-601.)</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathy, Hypertrophic - genetics</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Genes, MHC Class II - genetics</subject><subject>Genes, ras - genetics</subject><subject>Heart</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Muscle Proteins - genetics</subject><subject>Mutation</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Polymerase Chain Reaction</subject><subject>Proto-Oncogenes - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA-Directed DNA Polymerase</subject><subject>Sarcomeres - chemistry</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0d2L1DAQAPAgyrmePvskFBHf2pvJR9M8yrLeCScenuJjyKap7dltapJy7n9vvC33IAQSMr8ZJhlCXiNUiDVeAFZfd7dVw6q6Eoo_IRsUlJdcSHxKNgCgSskYPCcvYrwDQM6oOiNnSnIKgm9I3P2Zg4tx8FPhu-Im-ORLP1n_000uFmZqi8t8Kj4vyaQV3Zpg_cGFwT54N0yxGKbiJgM3pVj8GFJfXB1nF1Lwc5_Z1oR28Iejn03qjy_Js86M0b1a93Py_ePu2_aqvP5y-Wn74bq0XAIrqWw7FFa6vJSyjWwN7VoBlDZ7Y-geuHNMoayZ2zPBAFoKtqNCCoPYNsDOyftT3Tn434uLSR-GaN04msn5JWqZs4VSTYZv_4N3fglT7k1TpBxRUczo4oRs8DEG1-k5DAcTjhpB_5uFBtR5FrphutZ5FjnjzVp22R9c--jXz8_xd2vcRGvGLpjJDvGRUQ60BpkZP7F7PyYX4q9xuXdB986Mqdd5xMAAaYn5JZAbhfLhiv0FN1Khog</recordid><startdate>19980921</startdate><enddate>19980921</enddate><creator>Kai, Hisashi</creator><creator>Muraishi, Akihiko</creator><creator>Sugiu, Yuji</creator><creator>Nishi, Hirohumi</creator><creator>Seki, Yukihiko</creator><creator>Kuwahara, Fumitaka</creator><creator>Kimura, Akinori</creator><creator>Kato, Hirohisa</creator><creator>Imaizumi, Tsutomu</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>19980921</creationdate><title>Expression of Proto-oncogenes and Gene Mutation of Sarcomeric Proteins in Patients With Hypertrophic Cardiomyopathy</title><author>Kai, Hisashi ; Muraishi, Akihiko ; Sugiu, Yuji ; Nishi, Hirohumi ; Seki, Yukihiko ; Kuwahara, Fumitaka ; Kimura, Akinori ; Kato, Hirohisa ; Imaizumi, Tsutomu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4703-27df15c7ec7e99c87da2fd50228baa2b04ee391763eb35300d20cf2575a11d803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathy, Hypertrophic - genetics</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Genes, MHC Class II - genetics</topic><topic>Genes, ras - genetics</topic><topic>Heart</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Muscle Proteins - genetics</topic><topic>Mutation</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Polymerase Chain Reaction</topic><topic>Proto-Oncogenes - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA-Directed DNA Polymerase</topic><topic>Sarcomeres - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kai, Hisashi</creatorcontrib><creatorcontrib>Muraishi, Akihiko</creatorcontrib><creatorcontrib>Sugiu, Yuji</creatorcontrib><creatorcontrib>Nishi, Hirohumi</creatorcontrib><creatorcontrib>Seki, Yukihiko</creatorcontrib><creatorcontrib>Kuwahara, Fumitaka</creatorcontrib><creatorcontrib>Kimura, Akinori</creatorcontrib><creatorcontrib>Kato, Hirohisa</creatorcontrib><creatorcontrib>Imaizumi, Tsutomu</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kai, Hisashi</au><au>Muraishi, Akihiko</au><au>Sugiu, Yuji</au><au>Nishi, Hirohumi</au><au>Seki, Yukihiko</au><au>Kuwahara, Fumitaka</au><au>Kimura, Akinori</au><au>Kato, Hirohisa</au><au>Imaizumi, Tsutomu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Proto-oncogenes and Gene Mutation of Sarcomeric Proteins in Patients With Hypertrophic Cardiomyopathy</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1998-09-21</date><risdate>1998</risdate><volume>83</volume><issue>6</issue><spage>594</spage><epage>601</epage><pages>594-601</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Several mutations of cardiac beta-myosin heavy chain (beta-MHC) gene were reported in patients with hypertrophic cardiomyopathy (HCM). Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc expression in the steady-state myocardium on hypertrophic changes and to evaluate the possible interaction between beta-MHC mutation and proto-oncogene expression in HCM. Endomyocardial biopsy was performed in 17 HCM patients (5 beta-MHC mutations and 1 troponin T mutation) and 7 control subjects (no mutation). Reverse transcription-polymerase chain reaction analysis revealed c-H-ras expression in all members of both groups. Cardiomyocyte size was correlated with the expression level of c-H-ras (P<0.001), and c-H-ras expression was upregulated in HCM patients (P<0.01). HCM patients with a beta-MHC mutation had the higher c-H-ras expression than did control subjects or patients without a mutation (P<0.01). c-myc mRNA was expressed in 7 of 17 HCM patients but not in control subjects. Myocyte size was greater in c-myc-positive HCM patients than in control subjects and c-myc-negative HCM patients (P<0.001 and P<0.05, respectively). The proto-oncogene expression did not affect clinical findings, myocardial fibrosis, or disarray. In conclusion, c-H-ras and c-myc expression in the steady-state myocardium may play a role in the hypertrophic mechanism in HCM. It is possible that beta-MHC gene mutation has some effect on the regulation of proto-oncogene expression in HCM. (Circ Res. 1998;83:594-601.)</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9742054</pmid><doi>10.1161/01.RES.83.6.594</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete - AutoHoldings; EZB-FREE-00999 freely available EZB journals |
| subjects | Adolescent Adult Aged Biological and medical sciences Biopsy Cardiology. Vascular system Cardiomyopathy, Hypertrophic - genetics Female Gene Expression Genes, MHC Class II - genetics Genes, ras - genetics Heart Humans Male Medical sciences Middle Aged Muscle Proteins - genetics Mutation Myocarditis. Cardiomyopathies Myocardium - metabolism Myocardium - pathology Polymerase Chain Reaction Proto-Oncogenes - genetics RNA, Messenger - genetics RNA-Directed DNA Polymerase Sarcomeres - chemistry |
| title | Expression of Proto-oncogenes and Gene Mutation of Sarcomeric Proteins in Patients With Hypertrophic Cardiomyopathy |
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