Fig. 2

Nodal biological pathways identified as differentially regulated in the animal model of BPD. Differential gene expression analysis was further subjected to pathway enrichment analysis in order to delineate the underlying major biological signaling pathways that could be attributed to the protective effect seen in Sphk1 ^−/− mice against hyperoxia induced lung injury. The 7 M clusters of pathways were grouped by similar functions, thus highlighting significant differentially expressed genes most prevalent in our model, as shown here. The pathways combined to form clusters are described here. 1. Cell cycle metaphase check point (cluster 1), 2. DNA damage G2/M check point (cluster 3), 3. DNA-damage-induced apoptosis and survival (cluster 8), 4. Cell adhesion and extracellular matrix remodeling (cluster 10), 5. Pdgf signaling via NF-ĸB pathway (cluster 11a), 6. Wnt signaling and epithelial mesenchymal transition (cluster 11b), and 7. Sphingosine 1 phosphate (S1P) pathway (cluster 12). A detailed description of the pathways and how they were combined to form clusters is given in Additional file 2: Table S2