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Updated: Nov 30, 2025

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

Published on: June 24, 2020

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Perinatal inflammation alters histone 3 and histone 4 methylation patterns: Effects of MiR-29b supplementation

Sophia S Sugar1, Kathryn M Heyob1, Xinwei Cheng2

  • 1Center for Perinatal Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, USA.

Redox Biology
|November 17, 2020
PubMed

Insights

Maternal inflammation and neonatal hyperoxia cause epigenetic changes, including histone methylation suppression, linked to bronchopulmonary dysplasia. Restoring miR-29b partially reestablished histone methylation marks in a mouse model.

Area of Science:

  • Epigenetics
  • Neonatal Research
  • Pulmonary Medicine

Background:

  • Preterm birth remains a significant health concern.
  • Maternal inflammation and neonatal hyperoxia contribute to epigenetic alterations impacting gene expression and bronchopulmonary dysplasia (BPD) development.
  • Previous studies showed miR-29b suppression and increased DNA methylation in infants with severe BPD and in a mouse model.

Purpose of the Study:

  • To investigate histone methylation changes in a mouse model of maternal inflammation and neonatal hyperoxia.
  • To determine if restoring miR-29b expression could reverse observed histone methylation deficits.
  • To identify potential causes for decreased histone methylation.

Main Methods:

  • Utilized a murine model combining maternal inflammation and neonatal hyperoxia exposure.
  • Assessed global and specific histone methylation marks (H3K4me3, H3K27me3, H3K36me2, H3K79me2, H4K20me3).
  • Employed lipid nanoparticle delivery to restore miR-29b expression and evaluated the impact on histone methylation. Measured methylase and demethylase expression.

Main Results:

  • Exposed mice exhibited global suppression of histone methylation, with decreased expression of specific marks.
  • Restoration of miR-29b partially or fully reestablished H3K4me3, H3K27me3, and H4K20me3 methylation.
  • Decreased expression of the methylase SUV40H2, associated with H4K20me3, was observed.

Conclusions:

  • Maternal inflammation and neonatal hyperoxia induce significant global histone methylation suppression.
  • miR-29b restoration shows potential in reversing specific histone methylation deficits.
  • Further research is required to elucidate the mechanisms behind decreased histone methylation and explore therapeutic strategies for BPD.

Keywords:
HistoneHyperoxiaLung injuryMethylationmicroRNA

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