Supplementary Materials

Supplementary Material for:

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. E-mail: tmustoe{at}nm.org

Published 4 November 2015, Sci. Transl. Med. 7, 312ra177 (2015)
DOI: 10.1126/scitranslmed.aad0286

This PDF file includes:

  • Fig. S1. Nax immunostaining in keratinocytes.
  • Fig. S2. Expression of Nax and ENaC-α in mouse tissues (C57BL/6).
  • Fig. S3. Nax downstream gene expression in human primary keratinocytes, and knockdown and overexpression of Nax in HaCaT cells.
  • Fig. S4. The skin equivalent models used in the study.
  • Fig. S5. Immunofluorescence staining of Nax, prostasin, and ENaC-α.
  • Fig. S6. Change of the intracellular sodium concentrations in HaCaT cells.
  • Fig. S7. Expression of Nax, prostasin, and ENaC-α in stratified HaCaT cells.
  • Fig. S8. Cluster analysis of the protein kinase phosphorylation array.
  • Fig. S9. mRNA expression in WNK1 or p38α knockdown HaCaT cells treated with external serine protease.
  • Fig. S10. Activation of dermal fibroblasts was modulated by cocultured keratinocytes.
  • Fig. S11. Expression of prostasin in Nax-DsiRNA– or sham-DsiRNA–treated wounds was detected with its specific antibody and visualized with a fluorescently labeled secondary antibody.
  • Fig. S12. Inhibition of the Nax pathway by DsiRNA.
  • Fig. S13. Involvement of PAR-2 in the Nax pathway.
  • Fig. S14. Knockdown of Nax in HaCaT cells.
  • Table S1. Sequence information used for RNAi.
  • Table S2. Differentially expressed genes in wild-type and Nax knockdown keratinocytes under the stimulation with high sodium concentration.
  • Table S3. Sequence information for qPCR primers.

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