Related Experiment Video
Updated: May 12, 2025
08:02
Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
Published on: October 19, 2013
18.2K
VEGF-D Protects the Lung in Neonatal Hyperoxia-induced Lung Injury
Lakshanie C Wickramasinghe1, Elan L'Estrange-Stranieri1, Bailey Cardwell1
1Department of Immunology, School of Translational Medicine, Monash University, Melbourne, Victoria, Australia.
Summary
Supplemental oxygen worsens bronchopulmonary dysplasia (BPD) by damaging lungs. Fibroblast-derived VEGF-D is crucial for lymphatic development in BPD, and its absence exacerbates lung injury and inflammation.
Area of Science:
- Neonatal lung development and disease
- Vascular biology
- Fibroblast and lymphatic interactions
Background:
- Bronchopulmonary dysplasia (BPD) affects premature infants, with supplemental oxygen causing lung injury.
- Pulmonary vascular development is impaired in BPD, but lymphatic roles remain unclear.
Purpose of the Study:
- Investigate the role of vascular endothelial growth factor-D (VEGF-D) in neonatal lung response to hyperoxia.
- Define how fibroblasts and lymphatics are altered in BPD.
- Explore therapeutic targets for BPD.
Main Methods:
- Utilized a mouse model of hyperoxia-induced BPD.
- Analyzed single-cell RNA sequencing data for VEGF-D expression and fibroblast/lymphatic changes.
- Employed genetic deletion of Vegfd and qPCR to study mechanisms.
Main Results:
- Hyperoxia increased VEGF-D expression in lung fibroblasts.
- Alveolar fibroblasts showed altered transcriptional profiles under hyperoxia.
- Vegfd deficiency worsened BPD features, including alveolar simplification, edema, and inflammation, and disrupted lymphatic architecture.
Conclusions:
- Alveolar fibroblasts and VEGF-D are critical for lymphangiogenesis and lymphatic patterning in BPD.
- Targeting the fibroblast-VEGF-D-lymphatic axis may offer therapeutic strategies for BPD.
