Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?
Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and...
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| Veröffentlicht in: | Basic research in cardiology 2010-03, Vol.105 (2), p.219-226 |
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| creator | Conraads, Viviane M. Vrints, Christiaan J. Rodrigus, Inez E. Hoymans, Vicky Y. Van Craenenbroeck, Emeline M. Bosmans, Johan Claeys, Marc J. Van Herck, Paul Linke, Axel Schuler, Gerhard Adams, Volker |
| description | Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently ( |
| doi_str_mv | 10.1007/s00395-009-0068-5 |
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n
= 14) patients and from the Con (
n
= 12) group. MuRF-1/MAFbx expression was assessed using RT-PCR and Western blot (WB). In addition, the myocardial expression of TNF-α was measured (RT-PCR) and troponin I, β-myosin and phosphorylated Akt/Akt (pAkt/Akt) were quantified (WB). MuRF1 and MAFbx expression (mRNA and protein level) were significantly reduced in biopsies from MI patients. TNF-α was significantly higher in MI and exhibited a negative correlation with MuRF1 and MAFbx. The expression of troponin I and cardiomyocyte size were increased in MI in comparison to Con, whereas β-myosin expression was not altered. When compared with Con, pAkt/Akt was elevated. The results of the present study suggest that the atrogenes MuRF1/MAFbx are involved in regulating the hypertrophic response, characteristic of the early post-infarction remodeling phase. Reduced expression of MuRF1 and MAFbx in the myocardium might permit hypertrophy, which is supported by the elevation of troponin I. A regulatory role of TNF-α needs to be confirmed in further experiments.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-009-0068-5</identifier><identifier>PMID: 19859778</identifier><language>eng</language><publisher>Heidelberg: D. Steinkopff-Verlag</publisher><subject>Aged ; Biopsy ; Cardiology ; Coronary Artery Disease - metabolism ; Female ; Humans ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Muscle Proteins - metabolism ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardium - metabolism ; Myocardium - pathology ; Myocytes, Cardiac - pathology ; Original Contribution ; Proto-Oncogene Proteins c-akt - metabolism ; RNA, Messenger - metabolism ; Signal Transduction ; SKP Cullin F-Box Protein Ligases - metabolism ; Tripartite Motif Proteins ; Troponin I - metabolism ; Tumor Necrosis Factor-alpha - metabolism ; Ubiquitin-Protein Ligases - metabolism ; Ventricular Myosins - metabolism ; Ventricular Remodeling</subject><ispartof>Basic research in cardiology, 2010-03, Vol.105 (2), p.219-226</ispartof><rights>Springer-Verlag 2009</rights><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-aea10a42246dbbe765b019d3d494deb21d5f10fdeacd3dc619028e9e3d3459933</citedby><cites>FETCH-LOGICAL-c436t-aea10a42246dbbe765b019d3d494deb21d5f10fdeacd3dc619028e9e3d3459933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00395-009-0068-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-009-0068-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19859778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Conraads, Viviane M.</creatorcontrib><creatorcontrib>Vrints, Christiaan J.</creatorcontrib><creatorcontrib>Rodrigus, Inez E.</creatorcontrib><creatorcontrib>Hoymans, Vicky Y.</creatorcontrib><creatorcontrib>Van Craenenbroeck, Emeline M.</creatorcontrib><creatorcontrib>Bosmans, Johan</creatorcontrib><creatorcontrib>Claeys, Marc J.</creatorcontrib><creatorcontrib>Van Herck, Paul</creatorcontrib><creatorcontrib>Linke, Axel</creatorcontrib><creatorcontrib>Schuler, Gerhard</creatorcontrib><creatorcontrib>Adams, Volker</creatorcontrib><title>Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling?</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>Ventricular remodeling following myocardial infarction (MI) includes myocardial hypertrophy, a process requiring increased protein synthesis and sarcomere assembly. The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently (<2 weeks) infarcted regions (MI), compared with patients undergoing coronary artery bypass surgery, with normal systolic function and without previous infarction (control or Con). Left ventricular myocardial biopsies were obtained from the contralateral normal zone in MI (
n
= 14) patients and from the Con (
n
= 12) group. MuRF-1/MAFbx expression was assessed using RT-PCR and Western blot (WB). In addition, the myocardial expression of TNF-α was measured (RT-PCR) and troponin I, β-myosin and phosphorylated Akt/Akt (pAkt/Akt) were quantified (WB). MuRF1 and MAFbx expression (mRNA and protein level) were significantly reduced in biopsies from MI patients. TNF-α was significantly higher in MI and exhibited a negative correlation with MuRF1 and MAFbx. The expression of troponin I and cardiomyocyte size were increased in MI in comparison to Con, whereas β-myosin expression was not altered. When compared with Con, pAkt/Akt was elevated. The results of the present study suggest that the atrogenes MuRF1/MAFbx are involved in regulating the hypertrophic response, characteristic of the early post-infarction remodeling phase. Reduced expression of MuRF1 and MAFbx in the myocardium might permit hypertrophy, which is supported by the elevation of troponin I. A regulatory role of TNF-α needs to be confirmed in further experiments.</description><subject>Aged</subject><subject>Biopsy</subject><subject>Cardiology</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Muscle Proteins - metabolism</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Original Contribution</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>SKP Cullin F-Box Protein Ligases - metabolism</subject><subject>Tripartite Motif Proteins</subject><subject>Troponin I - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Ventricular Myosins - metabolism</subject><subject>Ventricular Remodeling</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kdFKHTEQhoNU9Gj7AN5I6E2vtk42ye7GmyK2pxaUQmmvQzaZ1ZXd5Jjsgj5DX7pZzwGlIEyYIfP9fwI_IScMPjOA-iwBcCULAJVP1RRyj6yY4LJgDfB3ZAUcoGhE2RySo5TuAZioKnZADplqpKrrZkX-fsVNxJTQUXx8nvrgaejozfxrzajxjt5crNtH2ntqIppEI45hwgWJaNFPdHwK1kTXmyFDnYl2yhbn1NAR7Z3xfRqpDX6KfTtPvb-lU3gtWewcDnnx5T3Z78yQ8MOuH5M_62-_L6-K65_ff1xeXBdW8GoqDBoGRpSlqFzbYl3JFphy3AklHLYlc7Jj0Dk0Nl_aiikoG1TIHRdSKc6Pyaet7yaGhxnTpMc-WRwG4zHMSdecV4zXTZnJj_-R92GOPn9Ol4yDzCUzxLaQjSGliJ3exH408Ukz0EtOepuTzjnpJSe9aE53xnM7ontR7ILJQLkFUl75W4wvL7_t-g-sUJ9Z</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Conraads, Viviane M.</creator><creator>Vrints, Christiaan J.</creator><creator>Rodrigus, Inez E.</creator><creator>Hoymans, Vicky Y.</creator><creator>Van Craenenbroeck, Emeline M.</creator><creator>Bosmans, Johan</creator><creator>Claeys, Marc J.</creator><creator>Van Herck, Paul</creator><creator>Linke, Axel</creator><creator>Schuler, Gerhard</creator><creator>Adams, Volker</creator><general>D. 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The anti-hypertrophic effect of MuRF1/MafBx, both muscle-specific E3-ubiquitin ligases, has been demonstrated in animal experiments and in cultured cardiomyocytes. We assessed MuRF1/MAFbx expression in myocardium remote of recently (<2 weeks) infarcted regions (MI), compared with patients undergoing coronary artery bypass surgery, with normal systolic function and without previous infarction (control or Con). Left ventricular myocardial biopsies were obtained from the contralateral normal zone in MI (
n
= 14) patients and from the Con (
n
= 12) group. MuRF-1/MAFbx expression was assessed using RT-PCR and Western blot (WB). In addition, the myocardial expression of TNF-α was measured (RT-PCR) and troponin I, β-myosin and phosphorylated Akt/Akt (pAkt/Akt) were quantified (WB). MuRF1 and MAFbx expression (mRNA and protein level) were significantly reduced in biopsies from MI patients. TNF-α was significantly higher in MI and exhibited a negative correlation with MuRF1 and MAFbx. The expression of troponin I and cardiomyocyte size were increased in MI in comparison to Con, whereas β-myosin expression was not altered. When compared with Con, pAkt/Akt was elevated. The results of the present study suggest that the atrogenes MuRF1/MAFbx are involved in regulating the hypertrophic response, characteristic of the early post-infarction remodeling phase. Reduced expression of MuRF1 and MAFbx in the myocardium might permit hypertrophy, which is supported by the elevation of troponin I. A regulatory role of TNF-α needs to be confirmed in further experiments.</abstract><cop>Heidelberg</cop><pub>D. Steinkopff-Verlag</pub><pmid>19859778</pmid><doi>10.1007/s00395-009-0068-5</doi><tpages>8</tpages></addata></record> |
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| ispartof | Basic research in cardiology, 2010-03, Vol.105 (2), p.219-226 |
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| subjects | Aged Biopsy Cardiology Coronary Artery Disease - metabolism Female Humans Male Medicine Medicine & Public Health Middle Aged Muscle Proteins - metabolism Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - pathology Original Contribution Proto-Oncogene Proteins c-akt - metabolism RNA, Messenger - metabolism Signal Transduction SKP Cullin F-Box Protein Ligases - metabolism Tripartite Motif Proteins Troponin I - metabolism Tumor Necrosis Factor-alpha - metabolism Ubiquitin-Protein Ligases - metabolism Ventricular Myosins - metabolism Ventricular Remodeling |
| title | Depressed expression of MuRF1 and MAFbx in areas remote of recent myocardial infarction: a mechanism contributing to myocardial remodeling? |
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