Fig. 7

Gene expression signature in the miR-30a^−/− female lung associated with human BPD blood transcriptomes. A The distributions of summed z-scores for the hyperoxia gene signatures from the four genotypes at PND21 were compared to the gene expression signatures obtained from the blood of human preterm neonates who developed BPD. In the human study, 111 preterm neonates of < 32 weeks gestation were included in the study. 43 neonates had no BPD, 40 had mild BPD, 13 had moderate and 15 had severe BPD. Disease severity was graded according to criteria proposed by Jobe and Bancalari [80]. Pearson correlation coefficient values are shown, correlating hyperoxia signatures to each clinical variable (gestational age, birth weight, BPD status, and oxygen requirement). B Distribution of summed z-scores (y-axis) for the murine lung hyperoxia signatures were correlated with the human newborn blood samples collected at PND28, stratified by biological sex and by BPD status (x-axis: BPD severity; no BPD, mild, moderate, and severe). Association was evaluated using the parametric Pearson correlation, with the Pearson correlation coefficient (r) and p-values indicated. C Selected Gene Ontology pathways and their normalized enrichment scores observed in the blood transcriptome of BPD patients at PND28, and the murine lung exposed to hyperoxia (WT and miR-30a^−/−). Biological pathways that were correlated between the miR-30a^−/− female lung signature with the human BPD patients, while modulated in the opposite direction in WT female lung are highlighted