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Jiang, D. ; de Vries, J.C.* ; Muschhammer, J.* ; Schatz, S.* ; Ye, H. ; Hein, T.* ; Fidan, M.* ; Romanov, V.S.* ; Rinkevich, Y. ; Scharffetter-Kochanek, K.*

Local and transient inhibition of p21 expression ameliorates age-related delayed wound healing.

Wound Repair Regen. 28, 49-60 (2020)
Postprint DOI PMC
Open Access Gold (Paid Option)
Wound Repair and Regeneration published by Wiley Periodicals, Inc. on behalf of by the Wound Healing Society. Nonhealing chronic wounds in the constantly growing elderly population represent a major public health problem with high socioeconomic burden. Yet, the underlying mechanism of age-related impairment of wound healing remains elusive. Here, we show that the number of dermal cells expressing cyclin-dependent kinase inhibitor p21 was elevated upon skin injury, particularly in aged population, in both man and mouse. The nuclear expression of p21 in activated wound fibroblasts delayed the onset of the proliferation phase of wound healing in a p53-independent manner. Further, the local and transient inhibition of p21 expression by in vivo delivered p21-targeting siRNA ameliorated the delayed wound healing in aged mice. Our results suggest that the increased number of p21+ wound fibroblasts enforces the age-related compromised healing, and targeting p21 creates potential clinical avenues to promote wound healing in aged population.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Cdkn1a ; Aging ; Fibroblasts ; P21 ; Wound Healing
ISSN (print) / ISBN 1067-1927
e-ISSN 1524-475X
Zeitschrift Wound repair and regeneration
Quellenangaben Band: 28, Heft: 1, Seiten: 49-60 Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Hoboken, NJ.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Lung Health and Immunity (LHI)
Förderungen Baustein Program from the Medical Faculty, University of Ulm
Fritz-Thyssen-Stiftung
German Research Foundation