{Reference Type}: Journal Article
{Title}: Tenascin-C modulates alveolarization in bronchopulmonary dysplasia.
{Author}: Liu W;Mao Y;Lv Q;Lu K;Yin C;Cheng R;Zhang M;
{Journal}: Inflamm Regen
{Volume}: 44
{Issue}: 1
{Year}: 2024 Mar 28
{Factor}: 10.426
{DOI}: 10.1186/s41232-024-00330-9
{Abstract}: Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by retarded alveolarization. Tenascin-C (TN-C), an extracellular matrix glycoprotein and soluble molecule, is involved in tissue morphogenesis. In the present study, we demonstrated that the level of TN-C in lung tissues was greater in a mouse model of BPD induced by 85% oxygen. TN-C deficiency, however, impaired alveolarization in the hyperoxia-induced BPD model. In contrast, a functional TN-C blocking antibody ameliorated alveolar dysplasia in BPD-like mice. Mechanistically, hyperoxia increased the soluble TN-C (sTN-C) released from respiratory epithelial cells. On one hand, low-dose sTN-C promoted lung epithelial cell proliferation and migration, which was mediated by ICAM-1. On the other hand, high-dose sTN-C hindered the proliferation and migration of epithelial cells. Overall, this study revealed that TN-C plays a dual role in lung alveolarization and that TN-C may be a target in BPD therapy.