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Updated: Apr 11, 2026

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

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PUMA-mediated mitochondrial apoptotic disruption by hypoxic postconditioning

YuZhen Li1, Qi Guo, XiuHua Liu

  • 1Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, 100853, China, yuzlif96@163.com.

Apoptosis : an International Journal on Programmed Cell Death
|June 6, 2015
PubMed

Insights

Hypoxic postconditioning protects heart cells from injury by reducing PUMA protein levels, thereby inhibiting the mitochondrial apoptosis pathway. This finding reveals a key mechanism for postconditioning

Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Mitochondrial Function

Background:

  • Ischemia-reperfusion (I/R) injury causes cardiomyocyte apoptosis, contributing to heart damage.
  • Mitochondria play a crucial role in the apoptotic process during I/R injury.
  • p53 upregulated modulator of apoptosis (PUMA) is implicated in lethal I/R injury.

Purpose of the Study:

  • To investigate whether hypoxic postconditioning inhibits mitochondrial pathway-mediated cardiomyocyte apoptosis by regulating PUMA expression.
  • To elucidate the role of PUMA in the cardioprotective effects of postconditioning.

Main Methods:

  • Neonatal rat cardiomyocytes were subjected to hypoxia and reoxygenation.
  • Postconditioning was induced using cycles of hypoxia and reoxygenation.
  • Levels of PUMA mRNA and protein were measured.
  • Mitochondrial membrane potential, cytochrome c release, and caspase-3 activation were assessed.
  • PUMA was overexpressed to evaluate its impact under postconditioning.

Main Results:

  • Hypoxic postconditioning significantly reduced PUMA mRNA and protein levels.
  • Postconditioning attenuated the loss of mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.
  • Overexpression of PUMA counteracted the protective effects of postconditioning, increasing apoptosis and mitochondrial dysfunction.

Conclusions:

  • Reduction of PUMA expression is a key mechanism underlying the cardioprotective effects of postconditioning.
  • Postconditioning disrupts the mitochondrial apoptotic pathway by modulating PUMA.
  • Targeting PUMA may offer a therapeutic strategy for mitigating I/R injury in the heart.

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