Fig. 5.

Deletion of miR-34a results in improvement of BPD. a NB WT (n = 8) and miR-34a KO (n = 11) mice were exposed to hyperoxia from PN day 1–15 and were monitored for survival. Survival data were analyzed using the Kaplan−Meier method and log-rank test. b Representative images of lung histology (H&E stain) of NB miR-34a KO mice exposed to RA or 100% O₂ at PN7. Scale bar: 100 µm. c Bar graph showing the morphometric analysis of lung histology sections of NB miR-34a KO mice exposed to RA or 100% O₂ at PN7. d, e Hyperoxia increased the numbers of neutrophils and BAL myeloperoxidase (MPO) in neonatal mouse lungs, and the deletion of miR-34a attenuated the hyperoxia-induced increase in neutrophil numbers in the BPD mouse model. f Representative H&E stained images of alveolar regions from lungs from WT and miR-34a KO mice from RA and BPD groups. g Morphometric analysis of lung histology sections of NB WT and miR-34a KO expressed as chord length and analyzed using Image J software. h Bar graph showing the percentage of TUNEL-positive cells indicating the apoptosis quantification in WT and miR-34a KO BPD models. i NB WT and miR-34a KO mice were exposed to hyperoxia from PN day 1−4. Western blots showing increased expression of Tie2, Ang1, SCF, and Notch2 in miR-34a KO lungs as compared to WT. j NB WT and miR-34a KO mice were exposed to hyperoxia from PN day 1−4. Western blots and quantification showing decreased expression of Ang2 in miR-34a KO lungs compared to WT, upon exposure to hyperoxia (n = 2). k Western blots and quantification of the same showing significantly decreased expression of Ang2 in miR-34a KO lungs as compared to WT, in the BPD model at PN14 (n = 3). BPD: bronchopulmonary dysplasia; NB: newborn; WT: Wild-type; KO: knockout or null mutant; PN or P: postnatal; BAL: bronchoalveolar lavage. Values are means ± SEM of a minimum of four animals in each group, unless otherwise stated. *P <0.05, **P <0.01, ***P <0.001, 2-way ANOVA, Tukey’s