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AKAP12 Upregulation Associates With PDE8A to Accelerate Cardiac Dysfunction.

Hanan Qasim1, Mehrdad Rajaei1, Ying Xu1

  • 1Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy (H.Q., M.R., Y.X., A.R.-A., H.Y.A., B.K.M.), University of Houston, TX.

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Upregulated AKAP12 in heart failure reduces cyclic adenosine 3

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Signaling via the β2-adrenergic receptor is crucial in heart failure, involving cyclic adenosine 3',5'-monophosphate (cAMP) and protein kinase A (PKA).
  • Phosphodiesterases (PDEs) regulate cAMP levels, and A kinase anchoring proteins (AKAPs) are potential therapeutic targets.
  • AKAP12, expressed in the heart, interacts with β2-adrenergic receptor, PKA, and PDE4D, but its cardiac function role is unknown.

Purpose of the Study:

  • To investigate the role of AKAP12 in cardiac function and its association with heart failure.
  • To elucidate the molecular mechanisms by which AKAP12 influences cardiac cell signaling.

Main Methods:

  • Real-time cAMP detection using a luciferase biosensor in AC16 cells overexpressing AKAP12.
  • Assessment of cardiomyocyte contractility and calcium handling in AKAP12-overexpressing mice treated with isoproterenol (ISO).
  • Evaluation of cardiac function and left ventricular size in mice after chronic ISO administration and analysis of AKAP12 expression in heart failure patients.

Main Results:

  • AKAP12 upregulation reduced intracellular cAMP levels via PDE8 in AC16 cells.
  • AKAP12-overexpressing cardiomyocytes showed impaired contractility and calcium handling, reversed by a PDE8 inhibitor.
  • AKAP12-overexpressing mice exhibited worsened systolic function and cardiac enlargement; AKAP12 was upregulated in end-stage heart failure patients.

Conclusions:

  • AKAP12 upregulation in cardiac tissue contributes to cardiac dysfunction.
  • The AKAP12-PDE8 axis is implicated in the accelerated cardiac dysfunction observed in heart failure.