EMF protects cardiomyocytes against hypoxia-induced injury via heat shock protein 70 activation

• EMF protects cardiomyocytes from hypoxia-induced injury.
• EMF exerted amelioration calcium homeostasis in hypoxic cardiomyocytes.
• EMF-induced cardioprotective mechanism via HSP70 activation in hypoxic cardiomyocytes.

Intracellular calcium (Ca2+i) overload induced by chronic hypoxia alters Ca2+i homeostasis, whereas ameliorating calcium homeostasis is believed to be responsible for cardioprotection. We hypothesize that cardioprotection by electromagnetic fields (EMF) exposure may restore Ca2+i homeostasis altered by hypoxia insults. Cardiomyocytes isolated from neonatal Sprague-Dawley rats were exposed to chronic hypoxia (1% O2, 5% CO2, 37 °C). We observed that cardiomyocytes injury and hypertrophy were alleviated in hypoxic cardiomyocytes exposed with EMF preconditioning. Compared with hypoxic cardiomyocytes, the diastolic [Ca2+]i was decreased, the amplitude of Ca2+i oscillations was recovered when cardiomyocytes exposed with EMF. In addition, we also found that EMF exposure significantly increased heat shock protein 70 (HSP70) mRNA expression in hypoxic cardiomyocytes. However, treatment with HSP70 blocker KNK437, almost completely inhibited the EMF induced-cardioprotection and the beneficial effects of Ca2+ oscillation in hypoxic cardiomyocytes. These results suggest that EMF preconditioning ameliorates Ca2+i homeostasis through activating HSP70, thereby producing the cardioprotective effect and reduction in hypoxic cardiomyocytes damage.