Regucalcin (SMP30) has been proposed to be involved in the maintenance of calcium homeostasis.
Although the expression of regucalcin was regulated in the liver and kidney during the embryogenesis and maturation
of these tissues, the roles of regucalcin were not defined yet in heart. This study focused on the investigation of
the differential expression changes in regucalcin and its function in hypoxic cardiomyocytes. The expression level
of regucalcin was the highest in 7 days after neonatal stage of rat heart. In hypoxic condition, reactive oxygen species
(ROS) production and calcium level were decreased in regucalcin-overexpressed cardiomyocytes about 60% compared
to normal cells. Regucalcin-transfected cells were slowly induced cell death in H2O2 treated condition and not
reduced proliferation in hypoxic condition. In proliferation-related signals, PKC-MEK1/2-ERK1/2 activation of
regucalcin-overexpressed cells was recovered in hypoxia, compared to hypoxic cardiomyocytes, and expression of
proto-oncogene was only affected c-myc by regucalcin. Transfected cardiomyocytes demonstrated that apoptotic
signal was hampered in regucalcin-regulated manner. In conclusion, these data suggest that regucalcin may regulate
proliferation and cell death in cardiomyocytes via calcium homeostasis.