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Epidermal-specific deletion of CD44 reveals a function in keratinocytes in response to mechanical stress

Shatirishvili, M. 1; Burk, A. S.; Franz, C. M. 2; Pace, G. 1; Kastilan, T. 1; Breuhahn, K.; Hinterseer, E.; Dierich, A.; Bakiri, L.; Wagner, E. F.; Ponta, H. 1; Hartmann, T. N.; Tanaka, M.; Orian-Rousseau, V. 1
1 Institut für Toxikologie und Genetik (ITG), Karlsruher Institut für Technologie (KIT)
2 Center for Functional Nanostructures (CFN), Karlsruher Institut für Technologie (KIT)

Abstract (englisch):

CD44, a large family of transmembrane glycoproteins, plays decisive roles in physiological and pathological conditions. CD44 isoforms are involved in several signaling pathways essential for life such as growth factor-induced signaling by EGF, HGF or VEGF. CD44 is also the main hyaluronan (HA) receptor and as such is involved in HA-dependent processes. To allow a genetic dissection of CD44 functions in homeostasis and disease, we generated a Cd44 floxed allele allowing tissue- and time-specific inactivation of all CD44 isoforms in vivo. As a proof of principle, we inactivated Cd44 in the skin epidermis using the K14Cre allele. Although the skin of such Cd44Δker mutants appeared morphologically normal, epidermal stiffness was reduced, wound healing delayed and TPA induced epidermal thickening decreased. These phenotypes might be caused by cell autonomous defects in differentiation and HA production as well as impaired adhesion and migration on HA by Cd44Δker keratinocytes. These findings support the usefulness of the conditional Cd44 allele in unraveling essential physiological and pathological functions of CD44 isoforms.


Volltext §
DOI: 10.5445/IR/1000062207
Originalveröffentlichung
DOI: 10.1038/cddis.2016.342
Scopus
Zitationen: 22
Web of Science
Zitationen: 23
Dimensions
Zitationen: 24
Cover der Publikation
Zugehörige Institution(en) am KIT Center for Functional Nanostructures (CFN)
Institut für Toxikologie und Genetik (ITG)
Universität Karlsruhe (TH) – Interfakultative Einrichtungen (Interfakultative Einrichtungen)
Publikationstyp Zeitschriftenaufsatz
Publikationsjahr 2016
Sprache Englisch
Identifikator ISSN: 2041-4889
urn:nbn:de:swb:90-622077
KITopen-ID: 1000062207
HGF-Programm 47.01.01 (POF III, LK 01) Biol.Netzwerke u.Synth.Regulat. ITG+ITC
Erschienen in Cell death & disease
Verlag Springer Nature [academic journals on nature.com]
Band 7
Seiten Article no: e2461
Bemerkung zur Veröffentlichung Gefördert durch den KIT-Publikationsfonds
Vorab online veröffentlicht am 10.11.2016
Nachgewiesen in Dimensions
Web of Science
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