Michalik, L; Desvergne, B; Tan, N S; Basu-Modak, S; Escher, Pascal; Rieusset, J; Peters, J M; Kaya, G; Gonzalez, F J; Zakany, J; Metzger, D; Chambon, P; Duboule, D; Wahli, W (2001). Impaired skin wound healing in peroxisome proliferator-activated receptor (PPAR)alpha and PPARbeta mutant mice. Journal of cell biology, 154(4), pp. 799-814. Rockefeller Institute Press 10.1083/jcb.200011148
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We show here that the alpha, beta, and gamma isotypes of peroxisome proliferator-activated receptor (PPAR) are expressed in the mouse epidermis during fetal development and that they disappear progressively from the interfollicular epithelium after birth. Interestingly, PPARalpha and beta expression is reactivated in the adult epidermis after various stimuli, resulting in keratinocyte proliferation and differentiation such as tetradecanoylphorbol acetate topical application, hair plucking, or skin wound healing. Using PPARalpha, beta, and gamma mutant mice, we demonstrate that PPARalpha and beta are important for the rapid epithelialization of a skin wound and that each of them plays a specific role in this process. PPARalpha is mainly involved in the early inflammation phase of the healing, whereas PPARbeta is implicated in the control of keratinocyte proliferation. In addition and very interestingly, PPARbeta mutant primary keratinocytes show impaired adhesion and migration properties. Thus, the findings presented here reveal unpredicted roles for PPARalpha and beta in adult mouse epidermal repair.
Item Type: |
Journal Article (Original Article) |
---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Ophthalmology |
UniBE Contributor: |
Escher, Pascal |
Subjects: |
600 Technology > 610 Medicine & health |
ISSN: |
0021-9525 |
Publisher: |
Rockefeller Institute Press |
Language: |
English |
Submitter: |
Pascal Escher |
Date Deposited: |
11 Jul 2017 08:45 |
Last Modified: |
05 Dec 2022 15:06 |
Publisher DOI: |
10.1083/jcb.200011148 |
PubMed ID: |
11514592 |
BORIS DOI: |
10.7892/boris.101792 |
URI: |
https://boris.unibe.ch/id/eprint/101792 |