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Published 20 August 2001. doi:10.1083/jcb.200011148
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© The Rockefeller University Press, 0021-9525/2001/8/799 $5.00
The Journal of Cell Biology, Volume 154, Number 4, August 20, 2001 799-814

Article

Impaired skin wound healing in peroxisome proliferator–activated receptor (PPAR){alpha} and PPARß mutant mice



Liliane Michalik1, Béatrice Desvergne1, Nguan Soon Tan1, Sharmila Basu-Modak1, Pascal Escher1, Jennifer Rieusset1, Jeffrey M. Peters3, Gürkan Kaya2, Frank J. Gonzalez3, Jozsef Zakany4, Daniel Metzger5, Pierre Chambon5, Denis Duboule4 and Walter Wahli1

1 Institut de Biologie Animale, Université de Lausanne, Bâtiment de Biologie, CH-1015 Lausanne, Switzerland
2 Department of Dermatology, University Hospital of Geneva, CH-1212 Geneva, Switzerland
3 Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institute of Health, Bethesda, MD 20892
4 Département de Zoologie, Université de Genève, Sciences III, CH-1211 Geneva 4, Switzerland
5 Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/ULP/Collège de France, 67404 Illkirch Cedex, CU de Strasbourg, France

Address correspondence to Walter Wahli, Institut de Biologie Animale, Université de Lausanne, Bâtiment de Biologie, CH-1015 Lausanne, Switzerland. Tel.: (41) 21-692-41-10. Fax: (41) 21-692-41-15. E-mail: walter.wahli{at}iba.unil.ch

We show here that the {alpha}, ß, 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, PPAR{alpha} and ß 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 PPAR{alpha}, ß, and {gamma} mutant mice, we demonstrate that PPAR{alpha} and ß are important for the rapid epithelialization of a skin wound and that each of them plays a specific role in this process. PPAR{alpha} is mainly involved in the early inflammation phase of the healing, whereas PPARß is implicated in the control of keratinocyte proliferation. In addition and very interestingly, PPARß mutant primary keratinocytes show impaired adhesion and migration properties. Thus, the findings presented here reveal unpredicted roles for PPAR{alpha} and ß in adult mouse epidermal repair.

Key Words: mouse keratinocytes; PPAR gene expression; PPAR gene targeted disruption; skin wound healing; nuclear hormone receptors


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