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Updated: Jan 21, 2026

Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs
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Development of a Neonatal Piglet Acute Lung Injury Model Recreating the Early Environment of Preterm Infant Lungs

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Hyperoxia causes miR199a-5p-mediated injury in the developing lung

Mohammad Afaque Alam1,2, Suhita Gayen Nee Betal3, Zubair H Aghai3

  • 1Department of Pediatrics, Division of Neonatology, Drexel University College of Medicine, Philadelphia, PA, USA.

Pediatric Research
|August 8, 2019
PubMed
Abstract

Insights

MicroRNA 199a-5p (miR199a-5p) is elevated in hyperoxia-induced acute lung injury (HALI) and bronchopulmonary dysplasia (BPD). Inhibiting miR199a-5p may offer a new therapy for developing lungs.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Neonatology

Background:

  • Hyperoxia-induced acute lung injury (HALI) impairs lung development and function.
  • MicroRNAs (miRs) are increasingly recognized for their role in HALI and bronchopulmonary dysplasia (BPD).
  • The specific role of miR199a-5p in developing lungs remains uncharacterized.

Purpose of the Study:

  • To investigate the expression profile and functional significance of miR199a-5p in developing lungs under hyperoxic conditions.
  • To explore the therapeutic potential of targeting miR199a-5p in HALI and BPD.

Main Methods:

  • Neonatal mice, lung epithelial cells (MLE12), endothelial cells (MLECs), and macrophages (RAW246.7) were exposed to hyperoxia.
  • miR199a-5p expression was analyzed in mouse lungs, cells, and infant tracheal aspirates.
  • Functional studies involved miR199a-5p mimics and inhibitors to assess effects on HALI markers.

Main Results:

  • miR199a-5p expression was significantly upregulated in hyperoxia-exposed lungs and cells, and in BPD infants.
  • Expression of caveolin-1, a target of miR199a-5p, was reduced.
  • miR199a-5p mimic administration exacerbated HALI, while miR199a-5p inhibitor treatment attenuated it.

Conclusions:

  • miR199a-5p plays a critical role in the pathophysiology of HALI in developing lungs.
  • Targeting miR199a-5p with inhibitors presents a promising therapeutic strategy for BPD in preterm neonates.

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