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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Mitochondrial K(ATP) channel activation reduces anoxic injury by restoring mitochondrial membrane potential

M Xu1, Y Wang, A Ayub

  • 1Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0529, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|August 22, 2001
PubMed

Insights

Mitochondrial ATP-sensitive K(+) channel activation protects heart cells from damage after ischemia-reperfusion injury. This channel activation prevents loss of mitochondrial membrane potential and inhibits apoptosis, crucial for cell survival.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Cellular Physiology

Background:

  • Ischemia-reperfusion (I-R) injury severely compromises myocardial mitochondrial membrane potential (DeltaPsi(m)).
  • Collapse of DeltaPsi(m) triggers apoptotic pathways, leading to myocyte death.
  • Mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels are potential targets for cardioprotection.

Purpose of the Study:

  • To test if mitoK(ATP) channel activation prevents DeltaPsi(m) collapse during anoxia-reoxygenation (A-R).
  • To determine if mitoK(ATP) channel activation protects myocytes by inhibiting apoptosis.
  • To investigate the role of mitoK(ATP) channels in preventing ischemia-reperfusion-induced cell injury.

Main Methods:

  • Cultured myocytes subjected to 3-h anoxia and 2-h reoxygenation (A-R).
  • Assessment of cell viability, membrane permeability, ATP levels, and apoptosis.
  • Mitochondrial integrity evaluated using Mito Tracker Orange, electron microscopy, and JC-1 staining for DeltaPsi(m).
  • Cytochrome c release assessed via immunostaining.
  • Effects of diazoxide (mitoK(ATP) activator) and 5-hydroxydecanoate (mitoK(ATP) inhibitor) evaluated.

Main Results:

  • A-R induced significant myocyte damage, decreased viability, increased apoptosis, and ATP depletion.
  • A-R led to mitochondrial swelling, DeltaPsi(m) collapse, and cytochrome c release.
  • Diazoxide treatment preserved DeltaPsi(m), reduced cytochrome c release, and protected against A-R injury.
  • The protective effect of diazoxide was abolished by 5-hydroxydecanoate, confirming mitoK(ATP) channel involvement.
  • Cyclosporin A prevented the opening of the mitochondrial permeability transition pore.

Conclusions:

  • Anoxia-reoxygenation disrupts mitochondrial membrane potential and induces apoptosis in myocytes.
  • Activation of the mitochondrial ATP-sensitive potassium channel by diazoxide prevents DeltaPsi(m) collapse and apoptosis.
  • MitoK(ATP) channel activation offers significant cardioprotection against ischemia-reperfusion injury, highlighting therapeutic potential.

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