Fig. 5

Loss of miR-30a led to significant changes in gene expression in the neonatal lung exposed to hyperoxia. A Number of differentially expressed genes in each genotype and sex in the hyperoxia-exposed lungs compared to room air controls. The number of up- and down-regulated genes shared between two or more genotypes, as well as the number of genes modulated in opposite directions between two or more genotypes, are depicted in the upset plot. B Correlation patterns of murine lung gene expression signatures scores over a large collection of healthy human lung transcriptomes. For studying the clustering of the lung transcriptome responses based on genotype and sex, we used transcriptome profiles of healthy human adult lung samples (n = 578) compiled by the GTEx consortium. Summed z-scores for each human individual and each genotype signature were computed and assessed for inter-signature correlations. The miR-30a^−/− female hyperoxia signature was clearly separated from the other signatures. C Pathway-based cluster analysis of gene expression signatures. Gene Set Enrichment Analysis (GSEA) was used to quantify the enrichment of GO Biological Process pathways, and hierarchical clustering and heatmaps were generated using the significant normalized enrichment scores (NES at FDR < 0.25). The miR-30a^−/− female hyperoxia signature clustered distinctly compared to the other signatures. D Biological pathways enriched in WT and miR-30a^−/− male and female lungs upon exposure to hyperoxia. The highlighted pathways were enriched in the miR-30a^−/− female but modulated in the opposite direction in the WT female lung