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-over expressed cardiomyocytes about 60% compared to normal cells. Regucalcin-transfected cells were slowly induced cell death in H 2O2 treated condition and not reduced proliferation in hypoxic condition. In proliferation-related signals, PKC-MEK1/2-ERK1/2 activation of regucalcin-over expressed 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.
|Number of pages||9|
|Journal||Tissue Engineering and Regenerative Medicine|
|Publication status||Published - 2009 Oct 1|
All Science Journal Classification (ASJC) codes
- Medicine (miscellaneous)
- Biomedical Engineering