Activators of Peroxisome Proliferator-Activated Receptors Protect Human Skin from Ultraviolet-B-Light-Induced Inflammation
Peroxisome proliferator-activated receptors (PPAR) are members of a nuclear receptor superfamily, which were initially described in the context of fatty acid degradation and adipocyte differentiation. In this study we tested the hypothesis that peroxisome proliferator-activated receptor activation a...
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| Veröffentlicht in: | Journal of investigative dermatology 2001-12, Vol.117 (6), p.1430-1436 |
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| creator | Kippenberger, Stefan Grundmann-Kollmann, Marcella Simon, Stephanie Dang, Tu-Anh Hardt-Weinelt, Katja Kaufmann, Roland Bernd, August Loitsch, Stefan Marcel |
| description | Peroxisome proliferator-activated receptors (PPAR) are members of a nuclear receptor superfamily, which were initially described in the context of fatty acid degradation and adipocyte differentiation. In this study we tested the hypothesis that peroxisome proliferator-activated receptor activation also controls inflammation. In an in vitro model with human keratinocytes inflammation was mimicked by irradiation with ultraviolet B light (150 mJ per cm2). Activators for PPAR-α (WY-14,643, clofibrate) were shown to reverse ultraviolet-B-light-mediated expression of inflammatory cytokines (interleukin-6, interleukin-8). An activator preferentially for PPAR-β (bezafibrate) did not show prominent effects on interleukin-6 and interleukin-8 expression. The anti-inflammatory action of WY-14,643 on skin cells was further demonstrated by in vivo testings in which topically applied WY-14,643 markedly increased the minimal erythema dose in ultraviolet-B-irradiated skin. Additionally, it was shown that ultraviolet B irradiation led to a decrease of all three peroxisome proliferator-activated receptor subsets at the mRNA level. Also transactivation of peroxisome proliferator response element was attenuated by ultraviolet B irradiation. The downregulation of peroxisome proliferator-activated receptors by ultraviolet B irradiation provides a possible mechanism that leads to exaggerated and prolonged inflammation. This work suggests the possibility of PPAR-α activators as novel nonsteroidal anti-inflammatory drugs in the topical treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and photodermatitis. |
| doi_str_mv | 10.1046/j.0022-202x.2001.01537.x |
| format | Article |
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In this study we tested the hypothesis that peroxisome proliferator-activated receptor activation also controls inflammation. In an in vitro model with human keratinocytes inflammation was mimicked by irradiation with ultraviolet B light (150 mJ per cm2). Activators for PPAR-α (WY-14,643, clofibrate) were shown to reverse ultraviolet-B-light-mediated expression of inflammatory cytokines (interleukin-6, interleukin-8). An activator preferentially for PPAR-β (bezafibrate) did not show prominent effects on interleukin-6 and interleukin-8 expression. The anti-inflammatory action of WY-14,643 on skin cells was further demonstrated by in vivo testings in which topically applied WY-14,643 markedly increased the minimal erythema dose in ultraviolet-B-irradiated skin. Additionally, it was shown that ultraviolet B irradiation led to a decrease of all three peroxisome proliferator-activated receptor subsets at the mRNA level. Also transactivation of peroxisome proliferator response element was attenuated by ultraviolet B irradiation. The downregulation of peroxisome proliferator-activated receptors by ultraviolet B irradiation provides a possible mechanism that leads to exaggerated and prolonged inflammation. This work suggests the possibility of PPAR-α activators as novel nonsteroidal anti-inflammatory drugs in the topical treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and photodermatitis.</description><identifier>ISSN: 0022-202X</identifier><identifier>EISSN: 1523-1747</identifier><identifier>DOI: 10.1046/j.0022-202x.2001.01537.x</identifier><identifier>PMID: 11886504</identifier><identifier>CODEN: JIDEAE</identifier><language>eng</language><publisher>Danvers, MA: Elsevier Inc</publisher><subject>Biological and medical sciences ; Cell Division - drug effects ; Cell Line, Transformed ; Dermatitis - metabolism ; DNA Primers ; Down-Regulation - radiation effects ; erythema ; Erythema - metabolism ; Gene Expression - immunology ; Gene Expression - radiation effects ; Humans ; Injuries of the skin. Diseases of the skin due to physical agents ; Interleukin-6 - genetics ; Interleukin-8 - genetics ; irradiation ; Keratinocytes - cytology ; Keratinocytes - metabolism ; Keratinocytes - radiation effects ; Medical sciences ; Peroxisome Proliferators - pharmacology ; PPAR ; Pyrimidines - pharmacology ; Receptors, Cytoplasmic and Nuclear - genetics ; Receptors, Cytoplasmic and Nuclear - metabolism ; Response Elements - physiology ; Skin - cytology ; Skin - immunology ; Skin - radiation effects ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Traumas. Diseases due to physical agents ; Ultraviolet Rays - adverse effects ; WY-14,643</subject><ispartof>Journal of investigative dermatology, 2001-12, Vol.117 (6), p.1430-1436</ispartof><rights>2001 The Society for Investigative Dermatology, Inc</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-8ab8a11dffb83ea4967be87fd55f9b95df88232186fe102f0553b82c495d13413</citedby><cites>FETCH-LOGICAL-c565t-8ab8a11dffb83ea4967be87fd55f9b95df88232186fe102f0553b82c495d13413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210369739?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,64384,64388,72240</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13399733$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11886504$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kippenberger, Stefan</creatorcontrib><creatorcontrib>Grundmann-Kollmann, Marcella</creatorcontrib><creatorcontrib>Simon, Stephanie</creatorcontrib><creatorcontrib>Dang, Tu-Anh</creatorcontrib><creatorcontrib>Hardt-Weinelt, Katja</creatorcontrib><creatorcontrib>Kaufmann, Roland</creatorcontrib><creatorcontrib>Bernd, August</creatorcontrib><creatorcontrib>Loitsch, Stefan Marcel</creatorcontrib><title>Activators of Peroxisome Proliferator-Activated Receptors Protect Human Skin from Ultraviolet-B-Light-Induced Inflammation</title><title>Journal of investigative dermatology</title><addtitle>J Invest Dermatol</addtitle><description>Peroxisome proliferator-activated receptors (PPAR) are members of a nuclear receptor superfamily, which were initially described in the context of fatty acid degradation and adipocyte differentiation. In this study we tested the hypothesis that peroxisome proliferator-activated receptor activation also controls inflammation. In an in vitro model with human keratinocytes inflammation was mimicked by irradiation with ultraviolet B light (150 mJ per cm2). Activators for PPAR-α (WY-14,643, clofibrate) were shown to reverse ultraviolet-B-light-mediated expression of inflammatory cytokines (interleukin-6, interleukin-8). An activator preferentially for PPAR-β (bezafibrate) did not show prominent effects on interleukin-6 and interleukin-8 expression. The anti-inflammatory action of WY-14,643 on skin cells was further demonstrated by in vivo testings in which topically applied WY-14,643 markedly increased the minimal erythema dose in ultraviolet-B-irradiated skin. Additionally, it was shown that ultraviolet B irradiation led to a decrease of all three peroxisome proliferator-activated receptor subsets at the mRNA level. Also transactivation of peroxisome proliferator response element was attenuated by ultraviolet B irradiation. The downregulation of peroxisome proliferator-activated receptors by ultraviolet B irradiation provides a possible mechanism that leads to exaggerated and prolonged inflammation. This work suggests the possibility of PPAR-α activators as novel nonsteroidal anti-inflammatory drugs in the topical treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and photodermatitis.</description><subject>Biological and medical sciences</subject><subject>Cell Division - drug effects</subject><subject>Cell Line, Transformed</subject><subject>Dermatitis - metabolism</subject><subject>DNA Primers</subject><subject>Down-Regulation - radiation effects</subject><subject>erythema</subject><subject>Erythema - metabolism</subject><subject>Gene Expression - immunology</subject><subject>Gene Expression - radiation effects</subject><subject>Humans</subject><subject>Injuries of the skin. Diseases of the skin due to physical agents</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-8 - genetics</subject><subject>irradiation</subject><subject>Keratinocytes - cytology</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - radiation effects</subject><subject>Medical sciences</subject><subject>Peroxisome Proliferators - pharmacology</subject><subject>PPAR</subject><subject>Pyrimidines - pharmacology</subject><subject>Receptors, Cytoplasmic and Nuclear - genetics</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Response Elements - physiology</subject><subject>Skin - cytology</subject><subject>Skin - immunology</subject><subject>Skin - radiation effects</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Traumas. 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In this study we tested the hypothesis that peroxisome proliferator-activated receptor activation also controls inflammation. In an in vitro model with human keratinocytes inflammation was mimicked by irradiation with ultraviolet B light (150 mJ per cm2). Activators for PPAR-α (WY-14,643, clofibrate) were shown to reverse ultraviolet-B-light-mediated expression of inflammatory cytokines (interleukin-6, interleukin-8). An activator preferentially for PPAR-β (bezafibrate) did not show prominent effects on interleukin-6 and interleukin-8 expression. The anti-inflammatory action of WY-14,643 on skin cells was further demonstrated by in vivo testings in which topically applied WY-14,643 markedly increased the minimal erythema dose in ultraviolet-B-irradiated skin. Additionally, it was shown that ultraviolet B irradiation led to a decrease of all three peroxisome proliferator-activated receptor subsets at the mRNA level. Also transactivation of peroxisome proliferator response element was attenuated by ultraviolet B irradiation. The downregulation of peroxisome proliferator-activated receptors by ultraviolet B irradiation provides a possible mechanism that leads to exaggerated and prolonged inflammation. This work suggests the possibility of PPAR-α activators as novel nonsteroidal anti-inflammatory drugs in the topical treatment of common inflammatory skin diseases such as atopic dermatitis, psoriasis, and photodermatitis.</abstract><cop>Danvers, MA</cop><pub>Elsevier Inc</pub><pmid>11886504</pmid><doi>10.1046/j.0022-202x.2001.01537.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Cell Division - drug effects Cell Line, Transformed Dermatitis - metabolism DNA Primers Down-Regulation - radiation effects erythema Erythema - metabolism Gene Expression - immunology Gene Expression - radiation effects Humans Injuries of the skin. Diseases of the skin due to physical agents Interleukin-6 - genetics Interleukin-8 - genetics irradiation Keratinocytes - cytology Keratinocytes - metabolism Keratinocytes - radiation effects Medical sciences Peroxisome Proliferators - pharmacology PPAR Pyrimidines - pharmacology Receptors, Cytoplasmic and Nuclear - genetics Receptors, Cytoplasmic and Nuclear - metabolism Response Elements - physiology Skin - cytology Skin - immunology Skin - radiation effects Transcription Factors - genetics Transcription Factors - metabolism Traumas. Diseases due to physical agents Ultraviolet Rays - adverse effects WY-14,643 |
| title | Activators of Peroxisome Proliferator-Activated Receptors Protect Human Skin from Ultraviolet-B-Light-Induced Inflammation |
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