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Related Experiment Videos

Myocardial stunning: association with altered gene expression

A S Wechsler1, J W Entwistle, M Ding

  • 1Department of Surgery, Medical College of Virginia, Richmond 23298-0645.

Journal of Cardiac Surgery
|May 1, 1994
PubMed
Summary

Myocardial ischemia and reperfusion induce heat shock 70 (HSP70) and c-fos gene expression. This response is linked to ischemia/reperfusion events, not cellular calcium loading or hypertrophy.

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Stress Response Mechanisms

Background:

  • Myocardial ischemia and reperfusion are known to trigger stress responses, including the expression of heat shock protein 70 (HSP70) and immediate early genes like c-jun, c-fos, and c-myc.
  • Previous studies could not definitively attribute these gene expression changes to ischemia, reperfusion, or superimposed hemodynamic stress due to model limitations.

Purpose of the Study:

  • To investigate the specific induction of stress response genes (c-fos, c-myc, hsp70) in a controlled model of isolated rat heart ischemia and reperfusion.
  • To differentiate the effects of ischemia and reperfusion from other potential stressors like abnormal hemodynamics or cellular calcium loading.

Main Methods:

  • Utilized a nonworking, isolated, blood-perfused rat heart model.

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  • Subjected the heart to varying durations of ischemia followed by reperfusion.
  • Quantified mRNA levels for c-fos, c-myc, and hsp70 using molecular techniques.
  • Also evaluated mRNA for the calcium/glucose-responsive stress protein GRP78.

    • Main Results:

    • Observed significant increases in hsp70 and c-fos mRNA expression, with expression levels correlating positively with the duration of ischemia.
    • Found no significant increase in c-myc mRNA levels under the experimental conditions.
    • Did not detect any increase in GRP78 mRNA, even in a model prone to cellular calcium loading.

    Conclusions:

    • The induction of hsp70 and c-fos mRNA is a direct consequence of myocardial ischemia and reperfusion.
    • These stress responses are independent of early hypertrophic signaling pathways, such as those triggered by afterload mismatching or calcium overload.
    • Further research is required to precisely delineate the independent contributions of ischemia versus reperfusion to the observed gene expression changes.