Abstract
Moderate levels of stress can be beneficial to health, while stress overload can cause injury or contribute to diseases. Despite a number of studies of adaptation or stress damage, the mechanisms of adaptation and stress damage remain far from clear. The effect and mechanisms of adaptation on cardiomyocytes damage caused by stress overload are discussed in this study. Data showed that mild repeated stress mitigated stress overload-induced cardiomyocyte injury both in an animal model of restraint stress and in H9C2 cells with GC (glucocorticoid) treatment. HSP70, HIP expression and interaction between HSP70 and HIP increased during adaptation induced by mild stress both in animals and H9C2 cells. Overexpression or inhibition of HSP70 in H9C2 cells with pCDNA-3.1-Hsp70 or KNK437 (HSP70 inhibitor) showed that HSP70 can protect H9C2 cells from GC-induced cell damage. A luciferase assay showed that Hsp70 plays its protective role through inhibition of GR transcription activity dependent on the interaction with HIP. These results indicated that HSP70 may promote adaptation with its interacting protein HIP, and increased levels of HSP70 and its interacting protein HIP during adaptation may play a protective role on stress-overload-induced cardiomyocyte injury.