Expression of connexins 40 and 43 in human left atrium in atrial fibrillation of different aetiologies
Objective: To test the hypothesis that atrial fibrillation (AF) is associated with changes in the expression of connexins 40 and 43 in the left atrium with more pronounced changes in mitral valve disease than in lone AF. Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in...
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| Veröffentlicht in: | Heart (British Cardiac Society) 2005-02, Vol.91 (2), p.166-170 |
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| creator | Wetzel, U Boldt, A Lauschke, J Weigl, J Schirdewahn, P Dorszewski, A Doll, N Hindricks, G Dhein, S Kottkamp, H |
| description | Objective: To test the hypothesis that atrial fibrillation (AF) is associated with changes in the expression of connexins 40 and 43 in the left atrium with more pronounced changes in mitral valve disease than in lone AF. Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in left atrial tissue of patients undergoing cardiac surgery. One group of patients had lone AF (n = 41), one group had AF and mitral valve repair (n = 36), and one group in sinus rhythm served as controls (n = 15). Results: Western blot analysis of connexin 40 and connexin 43 expression showed an increase of both gap junctional proteins (connexin 43 > connexin 40) in patients with AF of all forms compared with patients in sinus rhythm (p = 0.01 and p = 0.011, respectively). Subgroup analysis showed increased concentrations of connexin 40 in lone AF and AF with mitral valve disease compared with sinus rhythm (p = 0.06 and p = 0.029, respectively), whereas the same analysis for connexin 43 reached significance only in the mitral valve disease group (p = 0.031). No differences in connexin 40 and connexin 43 expression were detectable between lone AF and AF with mitral valve disease. Within the groups connexin 40 and connexin 43 expression did not differ between patients with paroxysmal AF and patients with chronic AF. Conclusion: The present study shows for the first time that AF can induce changes in the left atrium with increased connexin expression. Furthermore, no systematic differences between patients with paroxysmal and chronic AF were detected. |
| doi_str_mv | 10.1136/hrt.2003.024216 |
| format | Article |
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Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in left atrial tissue of patients undergoing cardiac surgery. One group of patients had lone AF (n = 41), one group had AF and mitral valve repair (n = 36), and one group in sinus rhythm served as controls (n = 15). Results: Western blot analysis of connexin 40 and connexin 43 expression showed an increase of both gap junctional proteins (connexin 43 > connexin 40) in patients with AF of all forms compared with patients in sinus rhythm (p = 0.01 and p = 0.011, respectively). Subgroup analysis showed increased concentrations of connexin 40 in lone AF and AF with mitral valve disease compared with sinus rhythm (p = 0.06 and p = 0.029, respectively), whereas the same analysis for connexin 43 reached significance only in the mitral valve disease group (p = 0.031). No differences in connexin 40 and connexin 43 expression were detectable between lone AF and AF with mitral valve disease. Within the groups connexin 40 and connexin 43 expression did not differ between patients with paroxysmal AF and patients with chronic AF. Conclusion: The present study shows for the first time that AF can induce changes in the left atrium with increased connexin expression. Furthermore, no systematic differences between patients with paroxysmal and chronic AF were detected.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/hrt.2003.024216</identifier><identifier>PMID: 15657225</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>Ablation ; Antibodies ; atrial fibrillation ; Atrial Fibrillation - etiology ; Atrial Fibrillation - metabolism ; Biological and medical sciences ; Blotting, Western ; CABG ; CAF ; Cardiac arrhythmia ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Cardiovascular disease ; Cardiovascular Medicine ; Case-Control Studies ; chronic atrial fibrillation ; connexin ; Connexin 43 - metabolism ; Connexins - metabolism ; coronary artery bypass grafting ; Coronary vessels ; Gap Junction alpha-5 Protein ; gap junctions ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; Heart ; Heart Atria ; Heart surgery ; HEPES ; human atrium ; Humans ; hydroxyethylpiperazine-ethanesulfonic acid ; Medical sciences ; Middle Aged ; Mitragyna ; mitral valve disease ; MVD ; Myocardium - metabolism ; PAF ; paroxysmal atrial fibrillation ; Patients ; Proteins ; sinus rhythm</subject><ispartof>Heart (British Cardiac Society), 2005-02, Vol.91 (2), p.166-170</ispartof><rights>Copyright 2005 by Heart</rights><rights>2005 INIST-CNRS</rights><rights>Copyright: 2005 Copyright 2005 by Heart</rights><rights>Copyright © Copyright 2005 by Heart 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b588t-d79a03d0805b0d7f0bb7016e7d847f96b26d6200f7d1d9729cda96d6aec64c673</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768705/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768705/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,27933,27934,53800,53802</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16443828$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15657225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wetzel, U</creatorcontrib><creatorcontrib>Boldt, A</creatorcontrib><creatorcontrib>Lauschke, J</creatorcontrib><creatorcontrib>Weigl, J</creatorcontrib><creatorcontrib>Schirdewahn, P</creatorcontrib><creatorcontrib>Dorszewski, A</creatorcontrib><creatorcontrib>Doll, N</creatorcontrib><creatorcontrib>Hindricks, G</creatorcontrib><creatorcontrib>Dhein, S</creatorcontrib><creatorcontrib>Kottkamp, H</creatorcontrib><title>Expression of connexins 40 and 43 in human left atrium in atrial fibrillation of different aetiologies</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Objective: To test the hypothesis that atrial fibrillation (AF) is associated with changes in the expression of connexins 40 and 43 in the left atrium with more pronounced changes in mitral valve disease than in lone AF. Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in left atrial tissue of patients undergoing cardiac surgery. One group of patients had lone AF (n = 41), one group had AF and mitral valve repair (n = 36), and one group in sinus rhythm served as controls (n = 15). Results: Western blot analysis of connexin 40 and connexin 43 expression showed an increase of both gap junctional proteins (connexin 43 > connexin 40) in patients with AF of all forms compared with patients in sinus rhythm (p = 0.01 and p = 0.011, respectively). Subgroup analysis showed increased concentrations of connexin 40 in lone AF and AF with mitral valve disease compared with sinus rhythm (p = 0.06 and p = 0.029, respectively), whereas the same analysis for connexin 43 reached significance only in the mitral valve disease group (p = 0.031). No differences in connexin 40 and connexin 43 expression were detectable between lone AF and AF with mitral valve disease. Within the groups connexin 40 and connexin 43 expression did not differ between patients with paroxysmal AF and patients with chronic AF. Conclusion: The present study shows for the first time that AF can induce changes in the left atrium with increased connexin expression. Furthermore, no systematic differences between patients with paroxysmal and chronic AF were detected.</description><subject>Ablation</subject><subject>Antibodies</subject><subject>atrial fibrillation</subject><subject>Atrial Fibrillation - etiology</subject><subject>Atrial Fibrillation - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>CABG</subject><subject>CAF</subject><subject>Cardiac arrhythmia</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Medicine</subject><subject>Case-Control Studies</subject><subject>chronic atrial fibrillation</subject><subject>connexin</subject><subject>Connexin 43 - metabolism</subject><subject>Connexins - metabolism</subject><subject>coronary artery bypass grafting</subject><subject>Coronary vessels</subject><subject>Gap Junction alpha-5 Protein</subject><subject>gap junctions</subject><subject>GAPDH</subject><subject>glyceraldehyde-3-phosphate dehydrogenase</subject><subject>Heart</subject><subject>Heart Atria</subject><subject>Heart surgery</subject><subject>HEPES</subject><subject>human atrium</subject><subject>Humans</subject><subject>hydroxyethylpiperazine-ethanesulfonic acid</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mitragyna</subject><subject>mitral valve disease</subject><subject>MVD</subject><subject>Myocardium - metabolism</subject><subject>PAF</subject><subject>paroxysmal atrial fibrillation</subject><subject>Patients</subject><subject>Proteins</subject><subject>sinus rhythm</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkc-L1DAUx4so7rp69iYB0YPQ2STNr14EGXZ2lEEPruItpE2yk7FNxqSV8b83pWVXvXjK471Pvu99-RbFcwRXCFXsch-HFYawWkFMMGIPinNEmCgxRN8e5rqitGSw4mfFk5QOEEJSC_a4OEOUUY4xPS_s1ekYTUoueBAsaIP35uR8AgQC5TUgFXAe7MdeedAZOwA1RDf2U3OqVAesa6LrOjUsEtpZa6LxGTW514VbZ9LT4pFVXTLPlvei-LK5ullvy92n6_frd7uyoUIMpea1gpWGAtIGam5h03CImOFaEG5r1mCmWfZruUa65rhutapzS5mWkZbx6qJ4O-sex6Y3us1nRNXJY3S9ir9kUE7-PfFuL2_DT4k4ExzSLPB6EYjhx2jSIHuXWpP9eRPGJPMOWlNIMvjyH_AQxuizuawlIGOcVThTlzPVxpBSNPbuFATllKDMCcopQTknmH-8-NPBPb9EloFXC6BSqzoblW9duucYIZXAInPlzLk0mNPdXMXvkwlO5ceva7n7_OHmervZyG3m38x80x_-e-Vvv9HBOw</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Wetzel, U</creator><creator>Boldt, A</creator><creator>Lauschke, J</creator><creator>Weigl, J</creator><creator>Schirdewahn, P</creator><creator>Dorszewski, A</creator><creator>Doll, N</creator><creator>Hindricks, G</creator><creator>Dhein, S</creator><creator>Kottkamp, H</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2005 by Heart</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050201</creationdate><title>Expression of connexins 40 and 43 in human left atrium in atrial fibrillation of different aetiologies</title><author>Wetzel, U ; Boldt, A ; Lauschke, J ; Weigl, J ; Schirdewahn, P ; Dorszewski, A ; Doll, N ; Hindricks, G ; Dhein, S ; Kottkamp, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b588t-d79a03d0805b0d7f0bb7016e7d847f96b26d6200f7d1d9729cda96d6aec64c673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Ablation</topic><topic>Antibodies</topic><topic>atrial fibrillation</topic><topic>Atrial Fibrillation - etiology</topic><topic>Atrial Fibrillation - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>CABG</topic><topic>CAF</topic><topic>Cardiac arrhythmia</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Medicine</topic><topic>Case-Control Studies</topic><topic>chronic atrial fibrillation</topic><topic>connexin</topic><topic>Connexin 43 - metabolism</topic><topic>Connexins - metabolism</topic><topic>coronary artery bypass grafting</topic><topic>Coronary vessels</topic><topic>Gap Junction alpha-5 Protein</topic><topic>gap junctions</topic><topic>GAPDH</topic><topic>glyceraldehyde-3-phosphate dehydrogenase</topic><topic>Heart</topic><topic>Heart Atria</topic><topic>Heart surgery</topic><topic>HEPES</topic><topic>human atrium</topic><topic>Humans</topic><topic>hydroxyethylpiperazine-ethanesulfonic acid</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mitragyna</topic><topic>mitral valve disease</topic><topic>MVD</topic><topic>Myocardium - metabolism</topic><topic>PAF</topic><topic>paroxysmal atrial fibrillation</topic><topic>Patients</topic><topic>Proteins</topic><topic>sinus rhythm</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wetzel, U</creatorcontrib><creatorcontrib>Boldt, A</creatorcontrib><creatorcontrib>Lauschke, J</creatorcontrib><creatorcontrib>Weigl, J</creatorcontrib><creatorcontrib>Schirdewahn, P</creatorcontrib><creatorcontrib>Dorszewski, A</creatorcontrib><creatorcontrib>Doll, N</creatorcontrib><creatorcontrib>Hindricks, G</creatorcontrib><creatorcontrib>Dhein, S</creatorcontrib><creatorcontrib>Kottkamp, H</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wetzel, U</au><au>Boldt, A</au><au>Lauschke, J</au><au>Weigl, J</au><au>Schirdewahn, P</au><au>Dorszewski, A</au><au>Doll, N</au><au>Hindricks, G</au><au>Dhein, S</au><au>Kottkamp, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of connexins 40 and 43 in human left atrium in atrial fibrillation of different aetiologies</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>91</volume><issue>2</issue><spage>166</spage><epage>170</epage><pages>166-170</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Objective: To test the hypothesis that atrial fibrillation (AF) is associated with changes in the expression of connexins 40 and 43 in the left atrium with more pronounced changes in mitral valve disease than in lone AF. Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in left atrial tissue of patients undergoing cardiac surgery. One group of patients had lone AF (n = 41), one group had AF and mitral valve repair (n = 36), and one group in sinus rhythm served as controls (n = 15). Results: Western blot analysis of connexin 40 and connexin 43 expression showed an increase of both gap junctional proteins (connexin 43 > connexin 40) in patients with AF of all forms compared with patients in sinus rhythm (p = 0.01 and p = 0.011, respectively). Subgroup analysis showed increased concentrations of connexin 40 in lone AF and AF with mitral valve disease compared with sinus rhythm (p = 0.06 and p = 0.029, respectively), whereas the same analysis for connexin 43 reached significance only in the mitral valve disease group (p = 0.031). No differences in connexin 40 and connexin 43 expression were detectable between lone AF and AF with mitral valve disease. Within the groups connexin 40 and connexin 43 expression did not differ between patients with paroxysmal AF and patients with chronic AF. Conclusion: The present study shows for the first time that AF can induce changes in the left atrium with increased connexin expression. Furthermore, no systematic differences between patients with paroxysmal and chronic AF were detected.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>15657225</pmid><doi>10.1136/hrt.2003.024216</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Ablation Antibodies atrial fibrillation Atrial Fibrillation - etiology Atrial Fibrillation - metabolism Biological and medical sciences Blotting, Western CABG CAF Cardiac arrhythmia Cardiac dysrhythmias Cardiology. Vascular system Cardiovascular disease Cardiovascular Medicine Case-Control Studies chronic atrial fibrillation connexin Connexin 43 - metabolism Connexins - metabolism coronary artery bypass grafting Coronary vessels Gap Junction alpha-5 Protein gap junctions GAPDH glyceraldehyde-3-phosphate dehydrogenase Heart Heart Atria Heart surgery HEPES human atrium Humans hydroxyethylpiperazine-ethanesulfonic acid Medical sciences Middle Aged Mitragyna mitral valve disease MVD Myocardium - metabolism PAF paroxysmal atrial fibrillation Patients Proteins sinus rhythm |
| title | Expression of connexins 40 and 43 in human left atrium in atrial fibrillation of different aetiologies |
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