Store-Operated Calcium Entry in Adult Wild Type Ventricle Cardiomyocytes

Abstract

Calcium is a one of the most important second messenger in cell, controlling a wide range of intracellular processes such as activation of transcriptional factors, metabolism, muscle contraction, apoptosis, proliferation etc. It has been reported that alterations in calcium homeostasis are associated with number of pathologies including neurodegenerative disorders, cardiac pathologies, muscular dystrophies and allergies. Store-operated calcium entry (SOCE) has been established as one of the most ubiquitous pathway of calcium entry in cells. The presence of SOCE has been shown both in excitable and non-excitable cells. It was discussed that SOCE may play a significant role in early development of postnatal cardiomyocytes. However, existence of functional SOCE in adult wild type cardiomyocytes remains controversial. Using a patch-clamp technique in whole-cell mode we recorded caffeine- and thapsigargin-induced calcium currents in primary culture of wild type ventricle cardiomyocytes isolated from adult mice. These currents could be partially blocked by classical SOCE inhibitor 2-APB at concentration of 50 mkM. Current-voltage relationships of 2-APB-sensitive fraction of the currents had a strong inward rectification that is typical for Ca2+ release-activated Ca2+ (CRAC) channels. The electrophysiological results were confirmed by fluorescent measurements with calcium dye Fura-2AM. Thus we for the first time obtained electrophysiological recordings of 2-APB-sensitive store-operated currents in adult wild type cardiomyocytes. These results can be used in the future studies for comparison of normal SOCE and SOCE in pathologies to establish SOCE as a possible novel target for medical treatment. The study was supported by RSF grant No 14-04-00720-P.