Fig. 6
From: Hyperoxia causes miR-34a-mediated injury via angiopoietin-1 in neonatal lungs

Inducible deletion of miR-34a from type 2 epithelial cells improves BPD. a Schematic of tamoxifen-induced deletion of miR-34a in Spc CRE-expressing miR-34a fl/fl mice. From the birth of NB pups, dams were injected with 2 mg tamoxifen IP for four consecutive days (PN1-PN5). For the BPD model pups were kept in the hyperoxia chamber for 4 days and both dams (alternating in RA and hyperoxia exposure every 24 h) were given tamoxifen. Representative bar graph showing tamoxifen deletion of miR-34a in Spc CRE positive miR-34 KO lungs (T2-miR34a −/−). b Representative graph shows chord length analysis of lung histology (H&E stain) of NB T2-miR34a −/−mice BPD model along with controls. c Bar graphs showing less TUNEL count of lung histology sections of NB T2-miR34a −/− mice BPD model, as compared to controls. d, e BAL neutrophils count and myeloperoxidase activity were reduced in NB T2-miR34a −/− mice BPD model, as compared to controls. BPD: bronchopulmonary dysplasia; Spc: surfactant protein c; NB: newborn; IP: intraperitoneal; PN: postnatal; RA; room air; KO: knockout or null mutant; T2: type 2 alveolar epithelial cells. Values are means ± SEM of a minimum four animals in each group. *P <0.05, **P <0.01, 2-way ANOVA, Tukey’s