Gene expression of human keratinocyte (HaCaT) under the stress of high sodium concentration

The mechanisms by which the epidermis responds to disturbances in barrier function and restores homeostasis are unknown. With a disruption of the epidermal barrier, water is lost resulting in an increase in extracellular sodium concentration. We demonstrate that the sodium channel Nax functions as the sodium sensor. With increased extracellular sodium, Nax up-regulates prostasin which results in activation of the sodium channel ENaC, resulting in increased sodium flux and increased downstream mRNA synthesis of inflammatory mediators. The same pathways are present in lung epithelial cells.

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Xu W, Hong SJ, Zhong A, Xie P, Jia S, Xie Z, Zeitchek M, Niknam-Bienia S, Zhao J, Porterfield DM, Surmeier DJ, Leung KP, Galiano RD, Mustoe TA