Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

• Published in: Inflammation and Regeneration 2024-03, Vol.44 (1), p.16-16
• Main Authors: Liu, Wei, Mao, Yu, Lv, Qianru, Lu, Keyu, Yin, Chunyu, Cheng, Rui, Zhang, Mingshun
• Format: Article
• Language: English
• Subjects: Bronchopulmonary dysplasia; Epithelial cells; Extracellular matrix; Hyperoxia; ICAM-1; Tenascin-C
• ISSN: 1880-9693; 1880-8190
• DOI: 10.1186/s41232-024-00330-9

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.