Sodium channel Nax is a regulator in epithelial sodium homeostasis

Wei Xu, Seok Jong Hong, Aimei Zhong, Ping Xie, Shengxian Jia, Zhong Xie, Michael Zeitchek, Solmaz Niknam-Bienia, Jingling Zhao, D. Marshall Porterfield, D. James Surmeier, Kai P. Leung, Robert D. Galiano, Thomas A. Mustoe*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


The mechanisms by which the epidermis responds to disturbances in barrier function and restores homeostasis are unknown. With a perturbation of the epidermal barrier, water is lost, resulting in an increase in extracellular sodium concentration. We demonstrate that the sodium channel Nax functions as a 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. Nax is present in multiple epithelial tissues, and up-regulation of its downstream genes is found in hypertrophic scars. In animal models, blocking Nax expression results in improvement in scarring and atopic dermatitis-like symptoms, both of which are pathological conditions characterized by perturbations in barrier function. These findings support an important role for Nax in maintaining epithelial homeostasis.

Original languageEnglish (US)
Article number312ra177
JournalScience translational medicine
Issue number312
StatePublished - Nov 4 2015

ASJC Scopus subject areas

  • General Medicine


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