Beschreibung:
<jats:title>Abstract</jats:title><jats:p>Wound repair is an orchestrated process, encompassing the phases of inflammation, proliferation and tissue remodeling. In this context, sodium hydrogen exchanger 1 (<jats:styled-content style="fixed-case">NHE</jats:styled-content>1) is crucial to epidermal barrier integrity and acidification. Recently, we found that extracellular <jats:styled-content style="fixed-case">pH</jats:styled-content> (<jats:styled-content style="fixed-case">pH</jats:styled-content>e) on wound surfaces is dramatically increased initially after barrier disruption, and that <jats:styled-content style="fixed-case">pH</jats:styled-content>e decreases gradually during physiological healing. Additionally, we have shown that spatial <jats:styled-content style="fixed-case">NHE</jats:styled-content>1‐patterns account for <jats:styled-content style="fixed-case">pH</jats:styled-content>e‐gradients on surfaces of chronic wounds. Here, we show that <jats:styled-content style="fixed-case">NHE</jats:styled-content>1‐expression is very low at margins initially after wounding and that it increases massively during the time‐course of physiolgical healing. This finding is in accordance with the decrease of <jats:styled-content style="fixed-case">pH</jats:styled-content>e on wound surfaces, which we reported on in previous works. Thus, we show that <jats:styled-content style="fixed-case">NHE</jats:styled-content>1 is an interesting target when it comes to modification of surface <jats:styled-content style="fixed-case">pH</jats:styled-content>e on wounds, both acute and chronic, and that <jats:styled-content style="fixed-case">NHE</jats:styled-content>1 is time‐dependently regulated in physiological healing.</jats:p>