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Developmental programming of O(2) sensing by neonatal intermittent hypoxia via epigenetic mechanisms

Jayasri Nanduri1, Nanduri R Prabhakar

  • 1Institute for Integrative Physiology and Center for Systems Biology of O(2) Sensing, Biological Science Division, University of Chicago, Chicago, USA.

Respiratory Physiology & Neurobiology
|August 1, 2012
PubMed

Insights

Neonatal intermittent hypoxia (IH) enhances carotid body and adrenal responses, persisting into adulthood. Epigenetic changes may offer therapeutic targets for preterm infants experiencing breathing issues.

Area of Science:

  • Cardiovascular Physiology
  • Neonatal Medicine
  • Neuroendocrinology

Background:

  • Recurrent apnea and intermittent hypoxia (IH) pose significant risks for preterm infants.
  • Carotid body chemoreceptors and adrenal medullary chromaffin cells (AMC) are crucial for maintaining cardiorespiratory stability during hypoxia.
  • Understanding the long-term effects of neonatal IH on these systems is vital for improving infant health outcomes.

Purpose of the Study:

  • To review the effects of neonatal intermittent hypoxia (IH) on oxygen sensing in the carotid body and adrenal medullary chromaffin cells (AMC) in neonatal rodents.
  • To explore the underlying mechanisms, including reactive oxygen species (ROS) and epigenetic modifications.
  • To identify potential therapeutic strategies for mitigating long-term cardiorespiratory morbidity in preterm infants.

Main Methods:

  • Review of studies investigating the impact of neonatal IH on carotid body sensory excitation and AMC catecholamine secretion in rodent models.
  • Analysis of the roles of reactive oxygen species (ROS), endothelin-1, and Ca(2+) signaling.
  • Examination of emerging evidence on epigenetic mechanisms, specifically DNA hypermethylation.

Main Results:

  • Neonatal IH potentiates hypoxia-evoked carotid body excitation and AMC catecholamine secretion.
  • These effects are mediated by ROS-dependent pathways involving endothelin-1 and Ca(2+) signaling.
  • The detrimental effects of neonatal IH extend into adulthood, linked to persistent ROS elevation and epigenetic changes like DNA hypermethylation.

Conclusions:

  • Neonatal IH induces lasting alterations in cardiorespiratory homeostasis mechanisms.
  • Epigenetic modifications, particularly DNA hypermethylation, contribute to the long-term increase in ROS levels.
  • DNA hypomethylating agents represent a promising therapeutic avenue to reduce long-term cardiorespiratory complications in preterm infants.

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