@article{discovery10068875,
         journal = {EMBO Molecular Medicine},
           title = {Targeting miR-34a/Pdgfra interactions partially corrects alveologenesis in experimental bronchopulmonary dysplasia},
            year = {2019},
            note = {This work is licensed under a Creative Commons Attribution 4.0 International License. The images
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           month = {February},
          volume = {11},
          number = {2},
        keywords = {Bronchopulmonary dysplasia, hyperoxia, lung development, miR-34a, platelet-derived growth factor},
             url = {https://doi.org/10.15252/emmm.201809448},
            issn = {1757-4684},
          author = {Ruiz-Camp, J and Quantius, J and Lignelli, E and Arndt, PF and Palumbo, F and Nardiello, C and Surate Solaligue, DE and Sakkas, E and Mi{\vz}{\'i}kov{\'a}, I and Rodr{\'i}guez-Castillo, JA and Vad{\'a}sz, I and Richardson, WD and Ahlbrecht, K and Herold, S and Seeger, W and Morty, RE},
        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){\ensuremath{\alpha}}-expressing myofibroblasts, a cell type critical for proper lung alveolarization. Global deletion of miR-34a; and inducible, conditional deletion of miR-34a in PDGFR{\ensuremath{\alpha}}+ cells afforded partial protection to the developing lung against hyperoxia-induced perturbations to lung architecture. Pdgfra mRNA was identified as the relevant miR-34a target, and using a target site blocker in�vivo, the miR-34a/Pdgfra interaction was validated as a causal actor in arrested lung development. An antimiR directed against miR-34a partially restored PDGFR{\ensuremath{\alpha}}+ 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/Pdgfra interaction to manage arrested lung development associated with preterm birth.}
}