The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes

Studies using PPARγ agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPARγ) is irrelevant to cutaneous photobiology. However, in several epithelial cell lines, ultraviolet B (UVB) has been shown to induce the nonenzymatic production of oxidized phospholip...

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Main Authors: Raymond L. Konger, Kellie Clay Martel, Danielle Jernigan, Qiwei Zhang, Jeffrey B. Travers
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2010/467053
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author Raymond L. Konger
Kellie Clay Martel
Danielle Jernigan
Qiwei Zhang
Jeffrey B. Travers
author_facet Raymond L. Konger
Kellie Clay Martel
Danielle Jernigan
Qiwei Zhang
Jeffrey B. Travers
author_sort Raymond L. Konger
collection DOAJ
description Studies using PPARγ agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPARγ) is irrelevant to cutaneous photobiology. However, in several epithelial cell lines, ultraviolet B (UVB) has been shown to induce the nonenzymatic production of oxidized phospholipids that act as PPARγ agonists. UVB is also a potent inducer of prostaglandin E2  (PGE2) production and COX-2 expression in keratinocytes and PPARγ is coupled to increased PGE2 production in other cell lines. In this current study, we demonstrate that PPARγ agonists, but not PPARα or PPARβ/δ agonists, induce PGE2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPARγ agonist-induced COX-2 expression and PGE2 production were partially inhibited by the PPARγ antagonist, GW9662, indicating that both PPARγ-dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPARγ is relevant to cutaneous photobiology in human epidermis.
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institution Kabale University
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series PPAR Research
spelling doaj-art-c8e2f8a4ce6142f0a4984a854a78d4662025-02-03T06:08:48ZengWileyPPAR Research1687-47571687-47652010-01-01201010.1155/2010/467053467053The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal KeratinocytesRaymond L. Konger0Kellie Clay Martel1Danielle Jernigan2Qiwei Zhang3Jeffrey B. Travers4Department of Pathology & Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USADepartment of Pathology & Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USADepartment of Pathology & Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USADepartment of Dermatology, Indiana University School of Medicine, Indianapolis, IN 46202, USADepartment of Dermatology, Indiana University School of Medicine, Indianapolis, IN 46202, USAStudies using PPARγ agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPARγ) is irrelevant to cutaneous photobiology. However, in several epithelial cell lines, ultraviolet B (UVB) has been shown to induce the nonenzymatic production of oxidized phospholipids that act as PPARγ agonists. UVB is also a potent inducer of prostaglandin E2  (PGE2) production and COX-2 expression in keratinocytes and PPARγ is coupled to increased PGE2 production in other cell lines. In this current study, we demonstrate that PPARγ agonists, but not PPARα or PPARβ/δ agonists, induce PGE2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPARγ agonist-induced COX-2 expression and PGE2 production were partially inhibited by the PPARγ antagonist, GW9662, indicating that both PPARγ-dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPARγ is relevant to cutaneous photobiology in human epidermis.http://dx.doi.org/10.1155/2010/467053
spellingShingle Raymond L. Konger
Kellie Clay Martel
Danielle Jernigan
Qiwei Zhang
Jeffrey B. Travers
The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
PPAR Research
title The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
title_full The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
title_fullStr The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
title_full_unstemmed The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
title_short The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced Prostaglandin E2 Production in Human Epidermal Keratinocytes
title_sort peroxisome proliferator activated receptor gamma system regulates ultraviolet b induced prostaglandin e2 production in human epidermal keratinocytes
url http://dx.doi.org/10.1155/2010/467053
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