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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
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Multifunctional Mitochondrial Epac1 Controls Myocardial Cell Death.

Loubina Fazal1, Marion Laudette1, Sílvia Paula-Gomes1

  • 1From the Inserm, UMR-1048, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France (L.F., M.L., S.P.-G., C.C., F.T., P.S., Y.S.-M., M.B., O.L., A.L., J.M.-P., F.L.); Université de Toulouse, France (L.F., M.L., S.P.-G., C.C., F.T., P.S., Y.S.-M., M.B., O.L., A.L., J.M.-P., F.L.); Inserm, U955, Equipe 03, F-94000, Créteil, France (S.P., B.G.), and Inserm, UMR-1046 (J.R., J.F.); and UMR CNRS-9214, PHYMEDEX, Université de Montpellier, France (J.R., J.F.).

Circulation Research
|January 19, 2017
PubMed
Summary

Mitochondrial Epac1 (exchange protein directly activated by cAMP 1) promotes cardiac cell death during ischemia/reperfusion injury. Inhibiting mitochondrial Epac1 protects the heart from damage, suggesting it as a therapeutic target.

Keywords:
calciumcyclic AMPischemia reperfusion injurymitochondriareactive oxygen species

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Signaling
  • Cardiac Pathophysiology

Background:

  • Cyclic AMP (cAMP) dysregulation contributes to cardiac disease.
  • Mitochondria are increasingly recognized as sites of cAMP production and signaling.
  • The precise role of mitochondrial cAMP signaling in cardiac pathophysiology remains unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial Epac1 (exchange protein directly activated by cAMP 1) in myocardial ischemia/reperfusion (I/R) injury.
  • To elucidate the molecular mechanisms by which MitEpac1 influences cardiomyocyte survival.

Main Methods:

  • Genetic ablation of Epac1 (Epac1-/-) in mice.
  • In vitro studies using adult cardiomyocytes subjected to hypoxia/reoxygenation.
  • Assessment of infarct size, cardiomyocyte apoptosis, and mitochondrial calcium handling.
  • Investigation of protein-protein interactions within mitochondria.

Main Results:

  • Epac1 genetic ablation protected against experimental myocardial I/R injury, reducing infarct size and cardiomyocyte apoptosis.
  • Epac1 inhibition prevented hypoxia/reoxygenation-induced cardiomyocyte death.
  • Mitochondrial Epac1 facilitates Ca2+ transfer between the endoplasmic reticulum and mitochondria, leading to overload and opening of the mitochondrial permeability transition pore.
  • MitEpac1 inhibits isocitrate dehydrogenase 2, reducing antioxidant capacity.

Conclusions:

  • Distinct cAMP-Epac1 microdomains exist within mitochondria, regulating myocardial cell death.
  • Epac1 emerges as a potential therapeutic target for mitigating ischemia-induced cardiac damage.