Fig. 5

The potential role of ICAM-1 in the proliferation of alveolar epithelial cells stimulated by low-dose sTN-C. 2 ng/mL sTN-C (a blank vector-transfected supernatant as a control) was used to activate MLE-12 cells in 24-well plates for 24 h. Total RNA was extracted using TRIzol, after which RNA sequencing was carried out. A Process diagram for transcriptome sequencing. B Bubble diagram of KEGG pathway enrichment. The AGE-RAGE signaling pathway was considerably increased in low-dose sTN-C-treated alveolar epithelial cells. C Volcano plot showing DEGs in sTN-C-treated alveolar epithelial cells. The upregulated genes are shown in red, and the downregulated genes are shown in green with a fold change > 1.0 and P < 0.05. ICAM-1 is marked with a special color. D The increase in ICAM-1 RNA expression was verified by qPCR. E ICAM-1 RNA expression in MLE-12 cells following 24 h of stimulation with 85% oxygen was measured by qPCR. F ICAM-1 RNA expression levels in the lung tissue of BPD model mice at P7 or P14 were measured via qPCR. G ICAM-1 protein expression in pulmonary tissues at P14 was measured by Western blotting. H In a model of alveolar epithelial cells stimulated with low-dose sTN-C, anti-ICAM-1 monoclonal antibodies (2 μg/mL) and isotype mouse IgG control antibodies (2 μg/mL) were added. The proliferation of MLE-12 cells was assessed using a CCK-8 assay