The peroxisome proliferator-activated receptor gamma system regulates ultraviolet B-induced prostaglandin e 2 production in human epidermal keratinocytes

Raymond Konger, Kellie Clay Martel, Danielle Jernigan, Qiwei Zhang, Jeffrey Travers

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5 Citations (Scopus)

Abstract

Studies using PPAR agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPAR ) 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 PPAR agonists. UVB is also a potent inducer of prostaglandin E 2 (PGE 2) production and COX-2 expression in keratinocytes and PPAR is coupled to increased PGE 2 production in other cell lines. In this current study, we demonstrate that PPAR agonists, but not PPAR or PPAR /δ agonists, induce PGE 2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPAR agonist-induced COX-2 expression and PGE 2 production were partially inhibited by the PPAR antagonist, GW9662, indicating that both PPAR -dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE 2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPAR is relevant to cutaneous photobiology in human epidermis.

Original languageEnglish
Article number467053
JournalPPAR Research
DOIs
StatePublished - 2010

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Prostaglandins B
PPAR gamma
Keratinocytes
Prostaglandins E
Photobiology
Epidermis
Skin
tert-Butylhydroperoxide
Cell Line

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Drug Discovery

Cite this

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title = "The peroxisome proliferator-activated receptor gamma system regulates ultraviolet B-induced prostaglandin e 2 production in human epidermal keratinocytes",
abstract = "Studies using PPAR agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPAR ) 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 PPAR agonists. UVB is also a potent inducer of prostaglandin E 2 (PGE 2) production and COX-2 expression in keratinocytes and PPAR is coupled to increased PGE 2 production in other cell lines. In this current study, we demonstrate that PPAR agonists, but not PPAR or PPAR /δ agonists, induce PGE 2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPAR agonist-induced COX-2 expression and PGE 2 production were partially inhibited by the PPAR antagonist, GW9662, indicating that both PPAR -dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE 2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPAR is relevant to cutaneous photobiology in human epidermis.",
author = "Raymond Konger and Martel, {Kellie Clay} and Danielle Jernigan and Qiwei Zhang and Jeffrey Travers",
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T1 - The peroxisome proliferator-activated receptor gamma system regulates ultraviolet B-induced prostaglandin e 2 production in human epidermal keratinocytes

AU - Konger, Raymond

AU - Martel, Kellie Clay

AU - Jernigan, Danielle

AU - Zhang, Qiwei

AU - Travers, Jeffrey

PY - 2010

Y1 - 2010

N2 - Studies using PPAR agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPAR ) 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 PPAR agonists. UVB is also a potent inducer of prostaglandin E 2 (PGE 2) production and COX-2 expression in keratinocytes and PPAR is coupled to increased PGE 2 production in other cell lines. In this current study, we demonstrate that PPAR agonists, but not PPAR or PPAR /δ agonists, induce PGE 2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPAR agonist-induced COX-2 expression and PGE 2 production were partially inhibited by the PPAR antagonist, GW9662, indicating that both PPAR -dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE 2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPAR is relevant to cutaneous photobiology in human epidermis.

AB - Studies using PPAR agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPAR ) 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 PPAR agonists. UVB is also a potent inducer of prostaglandin E 2 (PGE 2) production and COX-2 expression in keratinocytes and PPAR is coupled to increased PGE 2 production in other cell lines. In this current study, we demonstrate that PPAR agonists, but not PPAR or PPAR /δ agonists, induce PGE 2 production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPAR agonist-induced COX-2 expression and PGE 2 production were partially inhibited by the PPAR antagonist, GW9662, indicating that both PPAR -dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and tert-butylhydroperoxide- (TBH-) induced PGE 2 production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPAR is relevant to cutaneous photobiology in human epidermis.

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