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Am J Physiol Heart Circ Physiol 282: H1461-H1466, 2002; doi:10.1152/ajpheart.00447.2001
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Vol. 282, Issue 4, H1461-H1466, April 2002

Preconditioning prevents alterations in cardiac SR gene expression due to ischemia-reperfusion

Rana M. Temsah, Kenichi Kawabata, Donald Chapman, and Naranjan S. Dhalla

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6

We have previously shown that ischemic preconditioning (IP) improves cardiac performance and sarcoplasmic reticulum (SR) function in hearts subjected to ischemia-reperfusion (I/R). In this study, we examined the effect of IP on I/R-induced changes in gene expression for SR proteins such as the Ca2+ release channel, Ca2+ pump ATPase, phospholamban, and calsequestrin in the isolated rat heart. Normal isolated rat hearts exposed to three brief cycles of IP (5-min ischemia and 5-min reperfusion) exhibited a significant decrease in the transcript levels of SR genes. Nonpreconditioned I/R hearts when subjected to 30-min ischemia and 30-min reperfusion showed a marked decrease in mRNA levels for the SR proteins compared with normal hearts; this decrease was attenuated by preconditioning. Although hearts subjected to Ca2+ paradox (CP) have been shown to exhibit intracellular Ca2+ overload and SR dysfunction like those in I/R hearts, virtually nothing is known regarding the effect of CP on cardiac SR gene expression. Accordingly, CP (5-min Ca2+-free perfusion and 30-min reperfusion with normal medium) was observed to produce dramatic changes in SR gene expression, and the heart failed to contract; these alterations were attenuated by IP. Our results show that 1) both I/R and CP depress SR gene expression in the normal heart, 2) IP attenuates I/R- and CP-induced depression in cardiac function and SR gene expression, and 3) intracellular Ca2+ overload may play a role in depressing SR gene expression in both I/R and CP hearts.

ischemic preconditioning; ischemia-reperfusion; cardiac mRNA levels; Ca2+ paradoxic heart


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