Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

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 gr...

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Bibliographic Details
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
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Summary: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.
ISSN:1880-9693
1880-8190
DOI:10.1186/s41232-024-00330-9