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  4. Peroxisome proliferator-activated receptor (PPAR)-beta/delta stimulates differentiation and lipid accumulation in keratinocytes
 
research article

Peroxisome proliferator-activated receptor (PPAR)-beta/delta stimulates differentiation and lipid accumulation in keratinocytes

Schmuth, Matthias
•
Haqq, Christopher M.
•
Cairns, William J.
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2004
The Journal of investigative dermatology

Peroxisome proliferator-activated receptor (PPAR) are nuclear hormone receptors that are activated by endogenous lipid metabolites. Previous studies have demonstrated that PPAR-alpha activation stimulates keratinocyte differentiation in vitro and in vivo, is anti-inflammatory, and improves barrier homeostasis. Recent studies have shown that PPAR-beta/delta activation induces keratinocyte differentiation in vitro. This study demonstrated that topical treatment of mice with a selective PPAR-beta/delta agonist (GW1514) in vivo had pro-differentiating effects, was anti-inflammatory, improved barrier homeostasis, and stimulated differentiation in a disease model of epidermal hyperproliferation [corrected]. In contrast to PPAR-alpha activation, PPAR-beta/deltain vivo did not display anti-proliferative or pro-apoptotic effects. The pro-differentiating effects persisted in mice lacking PPAR-alpha, but were decreased in mice deficient in retinoid X receptor-alpha, the major heterodimerization partner of PPAR. Furthermore, in vitro PPAR-beta/delta activation, aside from stimulating differentiation-related genes, additionally induced adipose differentiation-related protein (ADRP) and fasting induced adipose factor (FIAF) mRNA in cultures keratinocytes, which was paralleled by increased oil red O staining indicative of lipid accumulation, the bulk of which were triglycerides (TG). Comparison of differentially expressed genes between PPAR-beta/delta and PPAR-alpha activation revealed distinct profiles. Together, these studies indicate that PPAR-beta/delta activation stimulates keratinocyte differentiation, is anti-inflammatory, improves barrier homeostasis, and stimulates TG accumulation in keratinocytes.

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Type
research article
DOI
10.1111/j.0022-202X.2004.22412.x
PubMed ID

15102088

Author(s)
Schmuth, Matthias
Haqq, Christopher M.
Cairns, William J.
Holder, Julie C.
Dorsam, Sheri
Chang, Sandra
Lau, Peggy
Fowler, Ashley J.
Chuang, Gary
Moser, Arthur H.
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Date Issued

2004

Published in
The Journal of investigative dermatology
Volume

122

Issue

4

Start page

971

End page

83

Subjects

Lipid Metabolism

Editorial or Peer reviewed

REVIEWED

Written at

OTHER

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LISP  
Use this identifier to reference this record
https://infoscience.epfl.ch/handle/20.500.14299/36725
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