| Literature DB >> 27249231 |
Sonja Haverkampf1, Judith Heider1, Katharina T Weiß1, Frank Haubner2, Tobias Ettl3, Julia Schreml4, Sarah Hedtrich5, Marietta von Süßkind-Schwendi6, Mark Berneburg1, Sigrid Karrer1, Joachim Dissemond7, Stephan Schreml1.
Abstract
Wound repair is an orchestrated process, encompassing the phases of inflammation, proliferation and tissue remodeling. In this context, sodium hydrogen exchanger 1 (NHE1) is crucial to epidermal barrier integrity and acidification. Recently, we found that extracellular pH (pHe) on wound surfaces is dramatically increased initially after barrier disruption, and that pHe decreases gradually during physiological healing. Additionally, we have shown that spatial NHE1-patterns account for pHe-gradients on surfaces of chronic wounds. Here, we show that NHE1-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 pHe on wound surfaces, which we reported on in previous works. Thus, we show that NHE1 is an interesting target when it comes to modification of surface pHe on wounds, both acute and chronic, and that NHE1 is time-dependently regulated in physiological healing.Entities:
Keywords: NHE1; Wound healing; sodium hydrogen exchanger-1; tissue repair
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Year: 2017 PMID: 27249231 DOI: 10.1111/exd.13097
Source DB: PubMed Journal: Exp Dermatol ISSN: 0906-6705 Impact factor: 3.960