[No authors listed]
Mechanical ventilation may cause ventilatorâinduced lung injury (VILI). Canonical Wnt signaling has been reported to serve an important role in the pathogenesis of VILI. Bioinformatics analysis revealed that canonical and nonâcanonical Wnt signaling pathways were activated in VILI. However, the role of nonâcanonical Wnt signaling in the pathogenesis of VILI remains unclear. The present study aimed to analyze the potential role of nonâcanonical Wnt signaling in VILI pathogenesis. Lung injury was assessed via Evans blue albumin permeability and histological scoring, as well as by inflammatory cytokine expression and total protein concentration in bronchoalveolar lavage fluid. The relative protein expression of canonical and nonâcanonical Wnt signaling pathway components were examined via western blotting and immunohistochemistry. The results demonstrated that 6Â h of mechanical ventilation at low tidal volume (LTV; 6Â ml/kg) or moderate tidal volume (MTV; 12Â ml/kg) induced lung injury in sensitive A/J mice. Ventilation with MTV increased the protein levels of Wntâinduced secreted protein 1 (WISP1), Rhoâassociated protein kinase 1 (ROCK1), phosphorylated (p)âRas homolog gene family, member A and pâCâJun Nâterminal kinase (JNK). Inhibition of ROCK1 by Y27632 and JNK by SP600125 attenuated MTVâinduced lung injury and decreased the expression of proteins involved in nonâcanonical Wnt signaling, including WISP1. In conclusion, nonâcanonical Wnt signaling participates in VILI by modulating WISP1 expression, which has been previously noted as critical for VILI development. Therefore, the nonâcanonical Wnt signaling pathway may provide a preventive and therapeutic target in VILI.
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