Literature DB >> 11839628

Altered expression of ADAMs (A Disintegrin And Metalloproteinase) in fibrillating human atria.

Marco Arndt1, Uwe Lendeckel, Christoph Röcken, Karen Nepple, Carmen Wolke, Antje Spiess, Christof Huth, Siegfried Ansorge, Helmut U Klein, Andreas Goette.   

Abstract

BACKGROUND: ADAMs (A Disintegrin And Metalloproteinase) are ectoproteases that have recently been reported to be expressed in cardiac tissue. Although they are known to regulate cell-cell and cell-matrix interactions, their pathophysiological role in various cardiac diseases is unclear. The purpose of the present study was to determine whether structural remodeling of the atria during atrial fibrillation (AF) is associated with altered ADAM expression. METHODS AND
RESULTS: Atrial tissue samples of 30 patients undergoing open-heart surgery were examined. Fifteen patients had persistent AF (> or =6 months), and the remaining 15 patients had no history of AF. ADAM9, ADAM10, and ADAM15 expression was analyzed quantitatively at the mRNA and protein levels. ADAM expression was localized by immunohistochemistry. ADAM expression was correlated with amounts of integrins beta1 and beta3. The amount of ADAM10 protein more than doubled during AF (82+/-15 versus 36+/-8 U; P<0.01). Amounts of ADAM15 protein (102+/-12 versus 40+/-6 U; P<0.01) and mRNA (24.0+/-5.6 versus 10.5+/-2.5 U; P<0.05) increased significantly during AF compared with sinus rhythm. ADAM9 protein was not detected in any sample. ADAM/integrin ratios showed an increase of 4- to 6-fold (P<0.05) in patients with AF who had significantly dilated atria (4.94+/-0.6 versus 4.3+/-0.7 cm; P<0.05). ADAM/integrin ratios correlated with atrial diameter.
CONCLUSIONS: AF is associated with an increase in the expression of ADAM10 and ADAM15. Enhanced ADAM-dependent disintegrin and metalloproteinase activity may be a molecular mechanism that contributes to the dilation of fibrillating human atria.

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Year:  2002        PMID: 11839628     DOI: 10.1161/hc0602.103639

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  19 in total

Review 1.  [New antiarrhythmic drugs for therapy of atrial fibrillation: I. Ion channel blockers].

Authors:  U Ravens; E Wettwer; U Schotten; R Wessel; D Dobrev
Journal:  Herzschrittmacherther Elektrophysiol       Date:  2006-06

2.  Expression of ADAM-15 in rat myocardial infarction.

Authors:  Ji Ke Li; Wen Juan Du; Shu Lin Jiang; Hai Tian
Journal:  Int J Exp Pathol       Date:  2009-06       Impact factor: 1.925

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Journal:  Cell Mol Life Sci       Date:  2019-06-17       Impact factor: 9.261

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Review 5.  EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: Definition, characterization, and clinical implication.

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Journal:  Heart Rhythm       Date:  2016-06-10       Impact factor: 6.343

6.  [Molecular biology of the heart atrium. New insights into the pathophysiology of atrial fibrillation as well as its clinical implications].

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Journal:  Z Kardiol       Date:  2004-11

Review 7.  A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.

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Review 8.  Disruptions and detours in the myocardial matrix highway and heart failure.

Authors:  Anne M Deschamps; Francis G Spinale
Journal:  Curr Heart Fail Rep       Date:  2005-03

9.  Histone-deacetylase inhibition reverses atrial arrhythmia inducibility and fibrosis in cardiac hypertrophy independent of angiotensin.

Authors:  Fang Liu; Mark D Levin; Nataliya B Petrenko; Min Min Lu; Tao Wang; Li Jun Yuan; Andrea L Stout; Jonathan A Epstein; Vickas V Patel
Journal:  J Mol Cell Cardiol       Date:  2008-09-16       Impact factor: 5.000

Review 10.  Atrial Calpains: Mediators of Atrialmyopathies in Atrial Fibrillation.

Authors:  Alicja Bukowska; Uwe Lendeckel; Andreas Goette
Journal:  J Atr Fibrillation       Date:  2014-04-30
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