The Peroxisome Proliferator-Activated Receptor Gamma System Regulates Ultraviolet B-Induced ProstaglandinE2Production in Human Epidermal Keratinocytes release_5tzdwfaklfdxlexailttrjzkvu

by Raymond L. Konger, Kellie Clay Martel, Danielle Jernigan, Qiwei Zhang, Jeffrey B. Travers

Published in PPAR Research by Hindawi Limited.

Volume 2010p1-8 (2010)

Abstract

Studies using PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>agonists in mouse skin have suggested that peroxisome proliferator-activated receptor gamma (PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>) 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<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>agonists. UVB is also a potent inducer of prostaglandin<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mtext>E</mml:mtext><mml:mn>2</mml:mn></mml:msub><mml:mrow><mml:mo>  </mml:mo><mml:mo>(</mml:mo><mml:mrow><mml:msub><mml:mrow><mml:mtext>PGE</mml:mtext></mml:mrow><mml:mn>2</mml:mn></mml:msub></mml:mrow><mml:mo>)</mml:mo></mml:mrow></mml:mrow></mml:math>production and COX-2 expression in keratinocytes and PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>is coupled to increased<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mrow><mml:mtext>PGE</mml:mtext></mml:mrow><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math>production in other cell lines. In this current study, we demonstrate that PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>agonists, but not PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>α</mml:mi></mml:math>or PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mrow><mml:mi>β</mml:mi><mml:mo>/</mml:mo><mml:mi>δ</mml:mi></mml:mrow></mml:mrow></mml:math>agonists, induce<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mrow><mml:mtext>PGE</mml:mtext></mml:mrow><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math>production and COX-2 expression in primary human keratinocytes (PHKs). Importantly, PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>agonist-induced COX-2 expression and<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mrow><mml:mtext>PGE</mml:mtext></mml:mrow><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math>production were partially inhibited by the PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>antagonist, GW9662, indicating that both PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>-dependent and -independent pathways are likely involved. GW9662 also suppressed UVB and<jats:italic>tert</jats:italic>-butylhydroperoxide- (TBH-) induced<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mrow><mml:mtext>PGE</mml:mtext></mml:mrow><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math>production in PHKs and intact human epidermis and partially inhibited UVB-induced COX-2 expression in PHKs. These findings provide evidence that PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math>is relevant to cutaneous photobiology in human epidermis.
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Type  article-journal
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Year   2010
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DOI  10.1155/2010/467053
PubMed  20508724
PMC  PMC2873656
Wikidata  Q33865064
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