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CREB activation and ischaemic preconditioning.

E Marais1, S Genade, A Lochner

  • 1Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, University of Stellenbosch, Tygerberg, Republic of South Africa.

Cardiovascular Drugs and Therapy
|January 22, 2008
PubMed
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Cyclic AMP responsive element-binding protein (CREB) phosphorylation is triggered by ischaemic preconditioning, involving p38 MAPK, ERK, PKA, and PKC. Reduced CREB phosphorylation during sustained ischaemia does not protect the heart.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Cellular Signalling

Background:

  • Ischaemic preconditioning protects the heart from injury.
  • p38 MAPK activation is a known trigger for preconditioning.
  • Downstream signalling pathways and effectors of preconditioning remain unclear.

Purpose of the Study:

  • Investigate signalling pathways leading to CREB phosphorylation during ischaemic or beta-adrenergic preconditioning.
  • Examine changes in CREB phosphorylation during sustained ischaemia and their role in ischaemia/reperfusion injury.

Main Methods:

  • Isolated perfused working rat heart model.
  • Preconditioning via 1x or 3x 5-min global ischaemia.
  • Pharmacological manipulation of CREB activation pathways.

Related Experiment Videos

  • Assessment of infarct size and CREB phosphorylation via Western blot.

    • Main Results:

    • Short ischaemia/reperfusion significantly increased CREB phosphorylation, mediated by catecholamines and adenosine.
    • PKA, PKC, ERK, and p38 MAPK activation are involved in preconditioning-induced CREB phosphorylation.
    • iPLA(2) and cPLA(2) activation also contribute to CREB phosphorylation; inhibition partially attenuated cardioprotection.
    • CREB phosphorylation decreased during sustained global ischaemia in both preconditioned and non-preconditioned hearts.

    Conclusions:

    • CREB phosphorylation during preconditioning may contribute to triggering cardioprotection.
    • Reduced CREB phosphorylation during sustained ischaemia is not associated with cardioprotection.