AI Article Synopsis
- Bronchopulmonary dysplasia (BPD) is a common issue in preterm infants causing ineffective gas exchange due to poor lung development, linked to elevated levels of miR-34a in myofibroblast cells.
- Deleting miR-34a in mouse models showed protective effects against lung damage caused by high oxygen levels, indicating its role in lung architecture disruption.
- Targeting the miR-34a pathway may offer new ways to improve lung development and treat BPD in preterm infants.
Article Abstract
Bronchopulmonary dysplasia (BPD) is a common complication of preterm birth characterized by arrested lung alveolarization, which generates lungs that are incompetent for effective gas exchange. We report here deregulated expression of miR-34a in a hyperoxia-based mouse model of BPD, where miR-34a expression was markedly increased in platelet-derived growth factor receptor (PDGFR)α-expressing myofibroblasts, a cell type critical for proper lung alveolarization. Global deletion of miR-34a; and inducible, conditional deletion of miR-34a in PDGFRα cells afforded partial protection to the developing lung against hyperoxia-induced perturbations to lung architecture. mRNA was identified as the relevant miR-34a target, and using a target site blocker , the miR-34a/ interaction was validated as a causal actor in arrested lung development. An antimiR directed against miR-34a partially restored PDGFRα myofibroblast abundance and improved lung alveolarization in newborn mice in an experimental BPD model. We present here the first identification of a pathology-relevant microRNA/mRNA target interaction in aberrant lung alveolarization and highlight the translational potential of targeting the miR-34a/ interaction to manage arrested lung development associated with preterm birth.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6404112 | PMC |
| http://dx.doi.org/10.15252/emmm.201809448 | DOI Listing |
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