Heat shock protein 70 expression in myocardium is blunted with simulated weightlessness

Exposure of cardiac cells to a mild thermal or ischaemic stress, sufficient to induce HSP expression, protects them against a subsequent exposure to a more severe ischaemic stress. Over expression of HSPs by transfection of herpes simplex virus vectors in vitro or in transgenic animal in vivo can protect primary cardiac cells from subsequent exposure to severe thermal or hypoxic stress. The increases in myocardial and liver HSP70 accumulation in response to nonexertional heat stress are attenuated with senescence, and hearts from aged animals exhibit an impaired ability to produce the protective HSP. In our previous work, peculiar changes associated with aging, like lipofuscin accumulation and collagen deposition were shown in the myocardial tissue of long-term simulated weightless rats. We therefore designed the present study to examine whether the heat-stress induced HSP70 accumulation in myocardial tissue may decline with simulated weightlessness.