Background: The aim of the present study was to examine whether stanniocalcin 1 (STC1) affects cardiomyocytes under physiological or pathophysiological conditions.
Methods and results: Using fresh isolated rat cardiomyocytes, the effects of STC1 on cell hypercontracture, cell shortening and Ca(2+) transients were measured after exposing the cells to ouabain. STC1 alone did not affect cell shortening or the Ca(2+) transient. Exposure to ouabain significantly increased the fraction of hypercontractured cells (40.5+/-1.4% vs 3.5+/-1.7% in the control, p<0.01). However, treatment with STC1 decreased the percentage of cell hypercontracture that was induced by ouabain, in a concentration-dependent manner (17.4+/-2.6% at 2.5 nmol/L STC1, p<0.01). Moreover, STC1 prevented the increase in diastolic intracellular Ca(2+) level that was induced by ouabain (-5.3+/-2.7% vs 7.9+/-3.7% induced by ouabain, p<0.05; -15.3+/-5.1% in the control) in the cardiomyocytes.
Conclusions: STC1 prevented the increase in diastolic Ca(2+) overload and ouabain-induced cell hypercontracture, which suggests that STC1 could effectively prevent cytosolic Ca(2+) overload and protect cardiomyocytes from pathophysiological conditions such as in the failing heart.