title: EMF protects cardiomyocytes against hypoxia-induced injury via heat shock protein 70 activation.
abstract: Intracellular calcium (Ca(2+)i) overload induced by chronic hypoxia alters Ca(2+)i homeostasis, whereas ameliorating calcium homeostasis is believed to be responsible for cardioprotection. We hypothesize that cardioprotection by electromagnetic fields (EMF) exposure may restore Ca(2+)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 [Ca(2+)]i was decreased, the amplitude of Ca(2+)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 Ca(2+) oscillation in hypoxic cardiomyocytes. These results suggest that EMF preconditioning ameliorates Ca(2+)i homeostasis through activating HSP70, thereby producing the cardioprotective effect and reduction in hypoxic cardiomyocytes damage.
authors.affiliation: The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, People's Republic of China.
authors.forename: Jinhong
authors.initials: J
authors.lastname: Wei
authors.affiliation: The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, People's Republic of China.
authors.forename: Jie
authors.initials: J
authors.lastname: Tong
authors.affiliation: The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, People's Republic of China.
authors.forename: Liying
authors.initials: L
authors.lastname: Yu
authors.affiliation: The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, People's Republic of China. Electronic address: zhangjb@mail.xjtu.edu.cn.
authors.forename: Jianbao
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001559:Benzhydryl Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D004574:Electromagnetic Fields; D005786:Gene Expression Regulation; D018840:HSP70 Heat-Shock Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D006706:Homeostasis; D000860:Hypoxia / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000528:radiation effects*; D011760:Pyrrolidinones / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism
chemical_list: D001559:Benzhydryl Compounds; D018840:HSP70 Heat-Shock Proteins; C410027:KNK 437; D011760:Pyrrolidinones; D002118:Calcium
keywords: Calcium homeostasis; Cardioprotection; EMF; HSP70; Hypoxia