ArticleStem cell research & therapy2024
Macrophage extracellular vesicle-packaged miR-23a-3p impairs maintenance and angiogenic capacity of human endothelial progenitor cells in neonatal hyperoxia-induced lung injury.
Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Bone Marrow Stem Cell Exosomes Protect Lung Cells from Oxygen Damage by Regulating miR-23a-3p/Slc7a2 Pathway.The journal of gene medicine · 2026Article
- Emerging therapeutic potential of umbilical cord-derived extracellular vesicles in lung-injurious diseases: a review of recent advances.Stem cell research & therapy · 2026Review
- Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling : EVs promote VSMC phenotypic switching.Cellular and molecular life sciences : CMLS · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Participation of miRNA-23a-3p in Pulmonary Tuberculosis Through Macrophages via the JAK-STAT Pathway.International journal of chronic obstructive pulmonary disease · 2026Article
- Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.Cell communication and signaling : CCS · 2025Article
- Safety, Efficacy and Bio-Distribution Analysis of Exosomes Derived From Human Umbilical Cord Mesenchymal Stem Cells for Effective Treatment of Bronchopulmonary Dysplasia by Intranasal Administration in Mice Model.International journal of nanomedicine · 2025Article
- Effect Analysis of Extracellular Vesicles in the Treatment of Bronchopulmonary Dysplasia via Different Drug Delivery and Administration Routes.International journal of nanomedicine · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundPremature infants requiring mechanical ventilation and supplemental oxygen for respiratory support are at increased risk for bronchopulmonary dysplasia (BPD), wherein inflammation have been proposed as a driver of hyperoxia-induced injuries, including persistent loss of endothelial progenitor cells (EPCs), impaired vascularization and eventual alveolar simplification in BPD lungs. However, the underlying mechanisms linking these phenomena remain poorly defined.
methodsWe used clodronate liposomes to deplete macrophages in a mouse model of neonatal hyperoxia-induced lung injury to evaluate if EPC loss in BPD lungs could be an effect of macrophage infiltration. We further generated in vitro culture systems initiated with cord blood (CB)-derived CD34
resultsInitial experiments using mouse model identified the crucial role of macrophage infiltration in eliciting significant reduction of c-Kit
conclusionOur findings highlight the importance of pulmonary intercellular communication in the pathophysiology of BPD, by identifying a linkage through vesicle transfer of miR-23a-3p from hyperoxic macrophages to EPCs, and thus demonstrating potential for novel therapeutic target in BPD.
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