Fig. 8.

miR-34a inhibition improves BPD phenotype via increased Ang1-Tie2 signaling. a Representative images of lung histology (H&E stain) of NB WT mice models of RA or BPD were treated with miR-34a inhibitor (20 µM; PN2 and PN4) intranasal. Scale bar: 100 µm. b, c Morphometric analyses of lung histology sections of NB WT mice miR-34a inhibitor at PN14. Alveolar size expressed as chord length and septal thickness. d Representative graph shows TUNEL-positive cells (%) in NB WT mice lungs treated with miR-34a inhibitor or control. e Western blot analysis of cleaved and total Caspase 3 was performed on MLE12 cells transfected with miR-34a inhibitor or scrambled control. f, g Bar graphs showing BAL neutrophils count and myeloperoxidase activity in RA and BPD mice treated with miR-34a inhibitor or scrambled control. h, i Bar graphs showing lung IL-1β and IL-6 in RA and BPD mice treated with miR-34a inhibitor or scrambled control. j Representative immunohistochemistry (IHC) images showing increased staining of PCNA in miR inhibitor treated PN4 hyperoxia exposed animals. Scale bar: 100 µm. k Western blot shows increased Ang1 and Tie2 in miR-34a inhibitor treated PN4 lung samples. BPD: bronchopulmonary dysplasia; Ang1: angiopoietin 1; NB: newborn; WT: wild-type; RA: room air; PN: postnatal; IL: interleukin. Values are means + SEM of a minimum of four observations (in vitro experiments) or four animals (in vivo experiments) in each group. *P <0.05, **P <0.01, ***P <0.01, compared with controls, 1-way ANOVA