© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
3,5,3'-Triiodothyronine deprivation affects phenotype and intracellular [Ca2+]i of human cardiomyocytes in culture
aIstituto di Fisiologia Clinica C.N.R., via Moruzzi 1, 56100 Pisa, Italy
bDipartimento di Patologia Sperimentale, Università di Pisa, Pisa, Italy
cScuola Normale Superiore, Pisa, Italy
dIstituto di Neurofisiologia C.N.R., Pisa, Italy
eOspedale Pediatrico Apuano, Divisione di Cardiochirurgia C.N.R., Massa, Italy
simona{at}ifc.cnr.it
paolicchi{at}biomed.unipi.it
tommaso{at}in.pi.cnr.it
gimmi{at}in.pi.cnr.it
saviozzim{at}biomed.unipi.it
anest{at}ifc.pi.cnr.it
iervasi{at}ifc.cnr.it
* Corresponding author. Tel.: +39-50-3152216; fax: +39-50-3152166
Objective: A decrease in plasma T3 concentration is a frequent finding in patients with heart failure. However, the role of this ‘low T3 syndrome’ on disease evolution has never been clarified. As phenotypic and functional cardiomyocyte impairments are alterations that correlate with the failing myocardium, we studied the long-term effects of T3 deprivation on human cardiomyocyte structure and calcium handling. Methods: Atrial cardiomyocytes and myocardial tissue were cultured with or without 3 nM T3. Microscopical examination of structural features was followed by analysis of 
-sarcomeric actinin and sarcoplasmic reticulum calcium ATP-ase (SERCA-2) content. Calcium handling was studied by [Ca2+]i imaging. Results: When stimulated with cyclopiazonic acid, a SERCA-2 inhibitor, T3-deprived cardiomyocytes showed significantly faster (P=0.03) and more transient (P=0.04) increases in [Ca2+]i than T3-supplemented cells. Moreover, in the T3-free cultures a significantly lower number of cells (P=0.003) responded to caffeine, a typical activator of sarcoplasmic reticulum Ca2+-release channel. T3-deprived cardiomyocytes also presented altered morphology with larger dimensions than T3-supplemented cells (P<0.0001). Additionally, in T3-deprived samples -sarcomeric actinin and SERCA-2 protein levels were reduced to 65.6±3% (P<0.0001) and 74.1±4% (P=0.005), respectively, when compared with the T3-supplemented group. Conclusions: Our data show that human cardiomyocyte calcium handling and phenotype are strongly influenced by T3 suggesting important implications of the ‘low T3 syndrome’ on the progression of heart failure.
KEYWORDS Cell culture/isolation; Myocytes; Hormones; Calcium (cellular); SR-function; Heart failure
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