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1 Renal /Medicine, Baylor College of Medicine, Houston, Texas, USA
2 Department of Pathology, University of Texas Health Sciences Center, Houston, Texas, USA
3 Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA
4 The Water and Salt Institute, University of Aarhus, Aarhus, Denmark
5 Cardiology/Medicine, University of Texas Health Sciences Center, Houston, Texas, USA
6 Cardiovascular Sciences Section, Baylor College of Medicine, Houston, Texas, USA
* To whom correspondence should be addressed. E-mail: sheikh{at}bcm.tmc.edu.
Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Since the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1)1 is expressed in the heart we reasoned that STC1 might play a role in the adaptive/maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using left ventricular assist device (LVAD) and compared the results to those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes, and arterial walls of failing hearts pre-LVAD, and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although, nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole-cell patch clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of trans-membrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart.
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