Why the study?
Does aging affect the induction of heat shock protein mRNA in response to transient ischemia in rat hearts?
Does aging affect the induction of heat shock protein mRNA in response to transient ischemia in rat hearts?
Aged rat hearts exhibit a defective sensing mechanism for ischemia, requiring a longer ischemic duration to induce protective heat shock protein mRNAs compared to young hearts.
Aged hearts may need longer ischemia for HSP induction; leaves open relevance to human ischemic tolerance and requires clinical validation.
Vulnerability of aged hearts to ischemia may be due to defects in protective mechanisms provided by heat shock proteins (HSPs). To determine whether there is a defect in the induction of HSPs by ischemia in old hearts, HSP72 and HSP73 (inducible and constitutive HSP70, respectively) mRNA induction was examined in young (2-mo-old; n = 36) and old (18-mo-old; n = 32) rat hearts. Transient (10- or 20-min) ischemia was applied by tightening a snare placed around left coronary arterial branches 3 days before examination to avoid the effect of operation on induction. HSP72 mRNA was induced markedly in young hearts after 10-min ischemia, peaked at 2 h, but was induced only slightly in old hearts. HSP73 mRNA was also induced in young hearts, peaked at 4 h, but was not induced in old hearts. The mRNAs were markedly induced in old hearts as well after 20-min ischemia, which was accompanied by the induction of HSP72 protein. Thus the age-related modulation of HSP72 and HSP73 mRNAs suggests a defective sensing mechanism for ischemia in old hearts.
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Nitta et al. (1994) studied this question.
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