title: NHE1 expression at wound margins increases time-dependently during physiological healing.
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.
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Sonja
authors.initials: S
authors.lastname: Haverkampf
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Judith
authors.initials: J
authors.lastname: Heider
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Katharina T
authors.initials: KT
authors.lastname: Weiß
authors.affiliation: Department of Otorhinolaryngology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Frank
authors.initials: F
authors.lastname: Haubner
authors.affiliation: Department of Maxillofacial Surgery, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Ettl
authors.affiliation: Institute for Human Genetics, University of Cologne, Cologne, Germany.
authors.forename: Julia
authors.initials: J
authors.lastname: Schreml
authors.affiliation: Department of Pharmacy, Freie Universität Berlin, Berlin, Germany.
authors.forename: Sarah
authors.initials: S
authors.lastname: Hedtrich
authors.affiliation: Department of Cardiothoracic Surgery, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Marietta
authors.initials: M
authors.lastname: von Süßkind-Schwendi
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Mark
authors.initials: M
authors.lastname: Berneburg
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Sigrid
authors.initials: S
authors.lastname: Karrer
authors.affiliation: Department of Dermatology, Venereology, and Allergology, University Medical Center Essen, Essen, Germany.
authors.forename: Joachim
authors.initials: J
authors.lastname: Dissemond
authors.affiliation: Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.
authors.forename: Stephan
authors.initials: S
authors.lastname: Schreml
mesh_terms: D004817:Epidermis / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D012333:RNA, Messenger / Q000378:metabolism*; D000074082:Sodium-Hydrogen Exchanger 1 / Q000235:genetics* / Q000378:metabolism*; D013997:Time Factors; D014945:Wound Healing
chemical_list: D012333:RNA, Messenger; C490998:SLC9A1 protein, human; D000074082:Sodium-Hydrogen Exchanger 1
keywords: NHE1; Wound healing; sodium hydrogen exchanger-1; tissue repair