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Am J Physiol Heart Circ Physiol (October 11, 2001). doi:10.1152/ajpheart.00660.2001
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Articles in PresS, published online ahead of print October 11, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00660.2001
Submitted on July 26, 2001
Accepted on October 4, 2001

Increased expression of a small heat shock protein (HSP27) protects adult canine ventricular myocytes from simulated ischemia/reperfusion injury

Richard S. Vander Heide1*

1 Pathology, John D. Dingell VAMC, Detroit, Michigan, USA; Pathology, Wayne State University Medical School, Detroit, Michigan, USA

* To whom correspondence should be addressed. E-mail: rvanderh{at}med.wayne.edu.

Previous studies have shown that adult rat myocytes can be protected from simulated ischemia-reperfusion (IR) injury by small heat shock proteins (sHSPs). However, to date the cardioprotective effect of sHSPs has not been confirmed in adult myocytes from a large animal species. Left ventricular myocytes from adult dogs were cultured and infected with a replication-deficient adenovirus designed to increase expression of the human form of HSP27. The response to simulated ischemia-reperfusion injury was compared using morphologic criteria. Virus-infected myocytes expressed 2-3 fold more HSP27 and sustained less injury in response to simulated IR than control cells (p< 0.001; paired t-test). Canine myocytes can be isolated, cultured and induced to increase the expression of a foreign protein without significant effects on differentiation and/or viability. Increased expression of HSP27 provides significant protection from simulated ischemia-reperfusion injury in adult canine myocytes. Determining the mechanism by which sHSPs protect from lethal cell injury will provide important new insights into the mechanism of irreversible cell injury in adult myocardium.




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