© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Immunolocalization of annexins IV, V and VI in the failing and non-failing human heart*
Center for Anesthesiology Research, The Cleveland Clinic Foundation and Department of Biology, Cleveland State University, 9500 Euclid Ave, FF40, Cleveland, OH 44195, USA
* Corresponding author. Tel.: +1-216-445-5045; fax: +1-216-445-4658 moravec{at}ccf.org
The failing human heart is characterized by changes in the expression and function of proteins involved in intracellular Ca2+ cycling, resulting in altered Ca2+ transients and impaired contractile properties of cardiac muscle. The role of the cardiac annexins in this process remains unclear. Annexins may play a role in the regulation of Ca2+ pumps and exchangers on the sarcolemma, and have been shown to be altered in some cardiac disease states. Objective: The goal of this study was to compare the immunolocalization and expression of annexins IV, V and VI in failing and non-failing human hearts. Methods: We used immunostaining to identify the subcellular location of annexins IV, V and VI proteins within the myocardial cell, and Western blot analysis to quantify the proteins in the same hearts. Results: Annexin IV showed a cytoplasmic distribution in both failing and non-failing human heart cells. Annexin V was localized at the z-line, around lipofuscin granules, and in the cytosol in the non-failing heart cells. Annexin VI was localized at the sarcolemma and intercalated disc. Protein levels of annexins IV and V were up-regulated in failing human hearts, while the expression of annexin VI was unchanged. Conclusions: Alterations in the intracellular localization of annexins, along with up-regulation of annexins IV and V in the failing human heart cells, suggests differential regulation of these Ca2+ regulatory proteins during heart failure.
KEYWORDS Ca-pump; Calcium (cellular); Cardiomyopathy; Heart failure; Sarcolemma
* Supported by NIH HL49929 and National AHA 95007700 and 95-261/EI.
1 Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Regulatory Biology at Cleveland State University.
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