Our results here show that gene delivery of MRCKα alone not only increased tight junction protein levels in healthy mice, but also restored ZO-1 and occludin expression and lung barrier function in pre-injured living lungs, indicating that downregulation of MRCKα might play a role in the pathogenesis of ARDS, and specifically, might be involved in the pulmonary barrier disruption. Here, OCLN is linked to acute respiratory distress syndrome.