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Verfasst von:Leibold, Julia [VerfasserIn]   i
 Riehl, Astrid [VerfasserIn]   i
 Hettinger, Jan [VerfasserIn]   i
 Durben, Michael [VerfasserIn]   i
 Heß, Jochen [VerfasserIn]   i
 Angel, Peter [VerfasserIn]   i
Titel:Keratinocyte-specific deletion of the receptor RAGE modulates the kinetics of skin inflammation in vivo
Verf.angabe:Julia S. Leibold, Astrid Riehl, Jan Hettinger, Michael Durben, Jochen Hess and Peter Angel
E-Jahr:2013
Jahr:16 May 2013
Umfang:7 S.
Fussnoten:Gesehen am 12.01.2022
Titel Quelle:Enthalten in: The journal of investigative dermatology
Ort Quelle:Amsterdam : Elsevier, 1938
Jahr Quelle:2013
Band/Heft Quelle:133(2013), 10 vom: Okt., Seite 2400-2406
ISSN Quelle:1523-1747
Abstract:The receptor for advanced glycation end products (RAGE) is a pattern recognition receptor causally related to the pathogenesis of acute and chronic inflammation. In a mouse model of inflammation-driven skin carcinogenesis, RAGE deletion conferred protection from the development of skin tumors due to a severely impaired cutaneous inflammation. Although the impact of RAGE expression in immune cells was shown to be essential for the maintenance of a cutaneous inflammatory reaction, the role of RAGE in keratinocytes remained unsolved. Using mice harboring a keratinocyte-specific deletion of RAGE, we analyzed its role in the regulation of an acute inflammatory response that was induced by topical treatment of the back skin with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA). We show that RAGE expression in cutaneous keratinocytes modulates the strength and kinetics of acute inflammation and supports the maintenance of epidermal keratinocyte activation. To address the underlying molecular mechanism, we isolated interfollicular epidermis by laser microdissection for gene expression analysis, and identified RAGE as a regulator in the temporal control of TPA-induced epidermal tumor necrosis factor alpha transcript levels. In summary, our data demonstrate that RAGE expression in keratinocytes is critically involved in the perpetuation of acute inflammation and support the central role of RAGE in paracrine communication between keratinocytes and stromal immune cells.
DOI:doi:10.1038/jid.2013.185
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1038/jid.2013.185
 Volltext: https://www.sciencedirect.com/science/article/pii/S0022202X15359996
 DOI: https://doi.org/10.1038/jid.2013.185
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1785831119
Verknüpfungen:→ Zeitschrift

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