BACKGROUND: Mitochondria are known to be a major target during ischemic cardiac 
injury. Previous studies have shown that in rodent myogenic cells and in the 
hearts of transgenic mice in which the heat shock or stress protein 70 is 
increased, there is a marked tolerance to ischemia/reperfusion injury. Two other 
heat shock proteins (HSP60 and HSP10) are known to form, within the 
mitochondria, a chaperonin complex that is important for mitochondrial protein 
folding and function. We were then interested in investigating whether increased 
expression of these two stress proteins is able to protect myogenic cells 
against ischemia/reperfusion injury.
METHODS AND RESULTS: We generated recombinant adenoviral vectors containing 
HSP60, HSP10, or a combination of the two genes. These adenoviral constructs 
overexpress significant amounts of these stress proteins in both rat neonatal 
cardiomyocytes and the myogenic H9 c2 cell line. Cells infected with an 
adenoviral construct overexpressing both HSP60 and HSP10 were found to be 
protected against simulated ischemia, whereas cells infected with adenoviral 
constructs overexpressing only HSP60 or HSP10 alone were not rendered tolerant 
to simulated ischemic injury.
CONCLUSIONS: These results suggest that the simultaneous expression of these two 
proteins that form a chaperonin complex in the mitochondria plays an important 
role in the survival of myogenic cells after ischemia/reperfusion injury.