Galectin-7 overexpression destroy airway epithelial barrier in transgenic mice.

When the integrity of airway epithelium is destroyed, the ordered airway barrier no longer exists and increase sensitivity to viral infections and allergens, leading to the occurrence of airway inflammation such as asthma. Here, we found that galectin-7 transgenic(+) mice exhibited abnormal airway structures as embryos and after birth. These abnormalities included absent or substantially reduced pseudostratified columnar ciliated epithelium and increased monolayer cells with irregular arrangement and widening of intercellular spaces. Moreover, airway tissue from galectin-7 transgenic(+) mice showed evidence of impaired cell-cell junctions and decreased expression of zonula occludens-1(ZO-1) and E-cadherin. When treated with respiratory syncytial virus (RSV) or ovalbumin (OVA), galectin-7 transgenic(+) mice developed substantially increased bronchial epithelial detachment and apoptosis, airway smooth muscle and basement membrane thickening, and enhanced airway responsiveness. We found that Galectin-7 localized in the cytoplasm and nucleus of bronchial epithelial cells, and that increased apoptosis was mediated through mitochondrial release of Cytochrome c, upregulated JNK1 activation and expression Caspase-3 in galectin-7 Tg(+) mice. These findings suggested that Galectin-7 cause airway structural defects and destroy airway epithelium barrier which predispose the airways to RSV or OVA-induced epithelial apoptosis, injury and other asthma responses. This article is protected by copyright. All rights reserved.