Since hyperoxia can lead to excessive production of TN-C protein in the lung tissues from BPD-like mice, we directly treated lung epithelial cells with hyperoxia (85% oxygen) and found that both human and mouse respiratory epithelial cells (BEAS-2B and MLE-12 cells) secreted more soluble TN-C after hyperoxia exposure (Fig. 3A-B). This evidence concerns the gene TNC and bronchopulmonary dysplasia.