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Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy
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Translatable mitochondria-targeted protection against programmed cardiovascular dysfunction

K J Botting1,2,3, K L Skeffington1,3, Y Niu1,2,3

  • 1Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.

Science Advances
|September 3, 2020
PubMed

Insights

Prenatal hypoxia programs offspring heart disease via mitochondrial oxidative stress. Antioxidant MitoQ intervention during development prevents this risk by enhancing nitric oxide signaling.

Area of Science:

  • Cardiovascular Science
  • Developmental Biology
  • Mitochondrial Medicine

Background:

  • Prenatal origins of heart disease are known, but human-comparable models are lacking.
  • Developmental hypoxia is a common pregnancy complication with long-term cardiovascular risks.
  • Translational research requires models with similar cardiovascular developmental milestones to humans.

Purpose of the Study:

  • To investigate cardiovascular dysfunction programmed by developmental hypoxia in sheep and chickens.
  • To test mitochondria-targeted antioxidant MitoQ as an intervention against hypoxia-induced cardiovascular risks.
  • To elucidate the molecular mechanisms underlying hypoxia-induced cardiovascular programming.

Main Methods:

  • In vivo and in vitro studies across organ, cellular, mitochondrial, and molecular levels.
  • Surgical techniques in sheep for fetal and adult cardiovascular function assessment.
  • Chicken embryo models to isolate developmental effects from maternal/placental influences.
  • MitoQ administration during hypoxic development.

Main Results:

  • Developmental hypoxia generates mitochondria-derived oxidative stress.
  • Hypoxia programs endothelial dysfunction and hypertension in adult offspring.
  • MitoQ treatment during development protected against cardiovascular risks.
  • Enhanced nitric oxide signaling was observed in MitoQ-treated offspring.

Conclusions:

  • Developmental hypoxia programs adult cardiovascular dysfunction through mitochondrial oxidative stress.
  • MitoQ is a potential therapeutic strategy to prevent prenatal hypoxia-induced heart disease.
  • Enhanced nitric oxide signaling mediates the protective effects of MitoQ.

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