Published online before print August 2, 2004, doi: 10.1161/01.CIR.0000138849.03311.C6
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(Circulation. 2004;110:770-775.)
© 2004 American Heart Association, Inc.
Original Articles |
Troponin I Isoform Expression in Human and Experimental Atrial Fibrillation
From the Cardiovascular Research Institute Maastricht, University Maastricht, Maastricht, Netherlands (V.L.J.L.T., J.A., M.A.A., M.B., G.J.J.M.v.E.); Department of Biomedical Sciences, University of Padova, Padova, Italy (L.G.); Department of Medical Physiology, University Medical Centre Utrecht, Utrecht, Netherlands (H.M.W.v.d.V.); and Department of Cardiology, Thoraxcenter University Hospital, University of Groningen, Groningen, Netherlands (I.C.V.).
Correspondence to V.L.J.L. Thijssen, PhD, Angiogenesis Laboratory, Department of Pathology, Academic Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, Netherlands. E-mail v.thijssen{at}path.unimaas.nl
Received November 18, 2003; de novo received January 26, 2004; revision received March 23, 2004; accepted April 9, 2004.
Background— Atrial fibrillation (AF) is accompanied by re-expression of fetal genes and activation of proteolytic enzymes. In this study both aspects were addressed with respect to troponin I (TnI) isoform expression.
Methods and Results— Western blotting and real-time reverse transcription–polymerase chain reaction were used to study TnI isoform expression in patients with paroxysmal or chronic AF and in goats after 1, 2, 4, 8, and 16 weeks of AF. In addition to cardiac TnI (cTnI), low expression of slow-twitch skeletal TnI (ssTnI) protein was found in 60% of patients in sinus rhythm or paroxysmal AF and in 8% of patients with chronic AF. In adult goat atrium, ssTnI protein expression was undetectable. Calcium-dependent degradation of cTnI protein was found in 1 or 2 of 6 animals after 1 to 4 weeks of AF. Although always low, ssTnI mRNA levels were significantly higher in patients who expressed ssTnI protein than in those who did not. Relative ssTnI mRNA expression was significantly lower in patients with paroxysmal AF and chronic AF than in those in sinus rhythm. In goats there was a tendency toward higher relative levels of ssTnI at the onset of AF followed by a normalization when AF had become sustained.
Conclusions— Atrial re-expression of ssTnI during paroxysmal AF in patients and during the first 2 weeks of pacing-induced AF in goats does not seem to be part of the process of AF-associated cardiomyocyte dedifferentiation but seems to result from transient cardiomyocyte stress at the onset of AF.
Key Words: atrial fibrillation • troponin I • myocytes, cardiac • gene expression • atrium
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