The role of placenta growth factor in the hyperoxia-induced acute lung injury in an animal model

• Published in: Cell biochemistry and function Vol. 33; no. 1; pp. 44 - 49
• Main Authors: Zhang, Liang, Yuan, Li-Jie, Zhao, Shuang, Shan, Yu, Wu, Hong-Min, Xue, Xin-Dong
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.01.2015; Wiley Subscription Services, Inc
• Subjects: acute lung injury; Acute Lung Injury - metabolism; alveolar type II cells; Animals; Animals, Newborn; Bronchoalveolar Lavage Fluid; Disease Models, Animal; Epithelial Cells; focal adhesion; focal adhesion kinase; Focal Adhesion Kinase 1 - metabolism; Focal Adhesions - metabolism; hyperoxia; Hyperoxia - metabolism; Lung - metabolism; Lung - pathology; Mice; neonates; Permeability; Placenta Growth Factor; placental growth factor; Pregnancy Proteins - metabolism; Rats; focal adhesion; placental growth factor; hyperoxia; focal adhesion kinase; alveolar type II cells; neonates; acute lung injury
• ISSN: 0263-6484; 1099-0844
• DOI: 10.1002/cbf.3085

Prolonged exposure to hyperoxia leads to acute lung injury. Alveolar type II cells are main target of hyperoxia‐induced lung injury. However, the cellular and molecular mechanisms remain unknown. Here, we aimed to investigate the role of placental growth factor (PLGF) in hyperoxia‐induced lung injury. Using experimental hyperoxia‐induced lung injury model of neonatal rat and mouse lung epithelial type II cells (MLE‐12), we examined the levels of PLGF in bronchoalveolar lavage fluid and in the supernatants of MLE‐12 cells. Our results revealed that exogenous PLGF induced hyperoxia‐induced lung injury. Furthermore, PLGF triggered a shift of vinculin from insoluble to soluble cell fraction, similar to the observation under hyperoxia stimulation. Moreover, we observed significantly reduced phosphorylation of focal adhesion kinase and increased permeability in MLE‐12 cells treated with PLGF. These results suggest that PLGF triggers focal adhesion disassembly in alveolar type II cells via inhibiting the activation of focal adhesion kinase. Our findings reveal a novel role of PLGF in hyperoxia‐induced lung injury and provide a potential target for the management of hyperoxia‐induced acute lung injury. Copyright © 2014 John Wiley & Sons, Ltd.