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      Nuclear Hormone Receptors and Mouse Skin Homeostasis: Implication of PPARβ

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          PPARβ is expressed in the mouse epidermis during fetal development, and progressively disappears from the interfollicular epidermis after birth. Interestingly, its expression is strongly reactivated in the adult epidermis in conditions where keratinocyte proliferation is induced and during wound healing. Data obtained on PPARβ heterozygous mice reveal that PPARβ is implicated in the control of keratinocyte proliferation and is necessary for rapid healing of a skin wound.

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          Most cited references 4

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          Peroxisome Proliferator-Activated Receptors: Nuclear Control of Metabolism

           B. Desvergne (1999)
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            Growth, adipose, brain, and skin alterations resulting from targeted disruption of the mouse peroxisome proliferator-activated receptor beta(delta).

            To determine the physiological roles of peroxisome proliferator-activated receptor beta (PPARbeta), null mice were constructed by targeted disruption of the ligand binding domain of the murine PPARbeta gene. Homozygous PPARbeta-null term fetuses were smaller than controls, and this phenotype persisted postnatally. Gonadal adipose stores were smaller, and constitutive mRNA levels of CD36 were higher, in PPARbeta-null mice than in controls. In the brain, myelination of the corpus callosum was altered in PPARbeta-null mice. PPARbeta was not required for induction of mRNAs involved in epidermal differentiation induced by O-tetradecanoylphorbol-13-acetate (TPA). The hyperplastic response observed in the epidermis after TPA application was significantly greater in the PPARbeta-null mice than in controls. Inflammation induced by TPA in the skin was lower in wild-type mice fed sulindac than in similarly treated PPARbeta-null mice. These results are the first to provide in vivo evidence of significant roles for PPARbeta in development, myelination of the corpus callosum, lipid metabolism, and epidermal cell proliferation.
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              Impaired skin wound healing in peroxisome proliferator–activated receptor (PPAR)α and PPARβ mutant mice

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

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                28 September 2001
                : 54
                : 5-6
                : 263-268
                aInstitut de Biologie Animale, Université de Lausanne, Bâtiment de Biologie, Lausanne, Switzerland; bDepartment of Pharmacy and Pharmacology, University of Bath, UK
                53269 Horm Res 2000;54:263–268
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 4, References: 13, Pages: 6


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