Heat shock protein 72 production and the protection effect for the cardiac fibroblast cells in response to cold shock treatment

Expression of heat shock proteins has been induced by several stimuli, e.g., hypoxia, ischemia, heat shock and drugs. It is not known whether cold shock induces heat shock stress proteins in the heart. The author employed isolated cultured cardiac cells to test the hypothesis that cold shock is a type of stress that induces heat shock proteins. Cultured cells from a rat heart were subjected to 30, 60 and 120 minutes of cold shock at 4 degrees Celsius followed by re-warming up to 37 degrees Celsius and incubated for 24 hours. Cells were isolated and expression of heat shock protein 72 was determined by Western blots. Results demonstrated significant expression of heat shock protein 72 in cold-shocked cells. This expression was dependent on the duration of the normothennic recovery after cold shock and showed the effect of protection from anoxic and re-oxygenation insult. These observations demonstrated that cold shock was cardioprotective following cold preservation and cardioplegic arrest. Heat shock protein induction played a role in this protection.