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Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists
Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production. In addition to cytokines, such as tumor necrosis factor‐alpha (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell l...
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Published in: | Photochemistry and photobiology 2010-07, Vol.86 (4), p.949-954 |
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description | Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production. In addition to cytokines, such as tumor necrosis factor‐alpha (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell lines have demonstrated that UVB‐mediated production of PAF agonists is due primarily to the pro‐oxidative effects of this stimulant, resulting in the nonenzymatic production of modified phosphocholines (oxidized glycerophosphocholines). The current studies use human skin to assess whether UVB irradiation generates PAF‐receptor agonists, and the role of oxidative stress in their production. These studies demonstrate that UVB irradiation of human skin results in PAF agonists, which are blocked by the antioxidant vitamin C and the epidermal growth factor receptor inhibitor PD168393. Inasmuch as UVB‐generated PAF agonists have been implicated in animal model systems as being involved in photobiologic processes including systemic immunosuppression and cytokine (TNF‐α) production, these studies indicate that this novel activity could be involved in human disease. |
doi_str_mv | 10.1111/j.1751-1097.2010.00743.x |
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In addition to cytokines, such as tumor necrosis factor‐alpha (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell lines have demonstrated that UVB‐mediated production of PAF agonists is due primarily to the pro‐oxidative effects of this stimulant, resulting in the nonenzymatic production of modified phosphocholines (oxidized glycerophosphocholines). The current studies use human skin to assess whether UVB irradiation generates PAF‐receptor agonists, and the role of oxidative stress in their production. These studies demonstrate that UVB irradiation of human skin results in PAF agonists, which are blocked by the antioxidant vitamin C and the epidermal growth factor receptor inhibitor PD168393. Inasmuch as UVB‐generated PAF agonists have been implicated in animal model systems as being involved in photobiologic processes including systemic immunosuppression and cytokine (TNF‐α) production, these studies indicate that this novel activity could be involved in human disease.</description><identifier>ISSN: 0031-8655</identifier><identifier>EISSN: 1751-1097</identifier><identifier>DOI: 10.1111/j.1751-1097.2010.00743.x</identifier><identifier>PMID: 20492565</identifier><identifier>CODEN: PHCBAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Antioxidants - pharmacology ; Apoptosis ; Ascorbic Acid - pharmacology ; Dose-Response Relationship, Radiation ; Experiments ; Free radicals ; Humans ; Kinases ; Lipids ; Mass spectrometry ; Oxidative Stress ; Phosphorylcholine - antagonists & inhibitors ; Phosphorylcholine - metabolism ; Phosphorylcholine - pharmacology ; Platelet Membrane Glycoproteins - agonists ; Proteins ; Quinazolines - pharmacology ; Reactive Oxygen Species - metabolism ; Receptors, G-Protein-Coupled - agonists ; Rodents ; Skin - metabolism ; Skin - radiation effects ; Time Factors ; Ultraviolet Rays</subject><ispartof>Photochemistry and photobiology, 2010-07, Vol.86 (4), p.949-954</ispartof><rights>2010 The Authors. Journal Compilation. The American Society of Photobiology</rights><rights>Copyright American Society for Photobiology Jul/Aug 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6673-2a91802980207741da6ebec6d6c031020164458da02aa997664ec1f43011026f3</citedby><cites>FETCH-LOGICAL-c6673-2a91802980207741da6ebec6d6c031020164458da02aa997664ec1f43011026f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20492565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Travers, Jared B.</creatorcontrib><creatorcontrib>Berry, Damien</creatorcontrib><creatorcontrib>Yao, Yongxue</creatorcontrib><creatorcontrib>Yi, Qiaofang</creatorcontrib><creatorcontrib>Konger, Raymond L.</creatorcontrib><creatorcontrib>Travers, Jeffrey B.</creatorcontrib><title>Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists</title><title>Photochemistry and photobiology</title><addtitle>Photochem Photobiol</addtitle><description>Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production. In addition to cytokines, such as tumor necrosis factor‐alpha (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell lines have demonstrated that UVB‐mediated production of PAF agonists is due primarily to the pro‐oxidative effects of this stimulant, resulting in the nonenzymatic production of modified phosphocholines (oxidized glycerophosphocholines). The current studies use human skin to assess whether UVB irradiation generates PAF‐receptor agonists, and the role of oxidative stress in their production. These studies demonstrate that UVB irradiation of human skin results in PAF agonists, which are blocked by the antioxidant vitamin C and the epidermal growth factor receptor inhibitor PD168393. Inasmuch as UVB‐generated PAF agonists have been implicated in animal model systems as being involved in photobiologic processes including systemic immunosuppression and cytokine (TNF‐α) production, these studies indicate that this novel activity could be involved in human disease.</description><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Dose-Response Relationship, Radiation</subject><subject>Experiments</subject><subject>Free radicals</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Mass spectrometry</subject><subject>Oxidative Stress</subject><subject>Phosphorylcholine - antagonists & inhibitors</subject><subject>Phosphorylcholine - metabolism</subject><subject>Phosphorylcholine - pharmacology</subject><subject>Platelet Membrane Glycoproteins - agonists</subject><subject>Proteins</subject><subject>Quinazolines - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Rodents</subject><subject>Skin - metabolism</subject><subject>Skin - radiation effects</subject><subject>Time Factors</subject><subject>Ultraviolet Rays</subject><issn>0031-8655</issn><issn>1751-1097</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqNkm9v0zAQxi0EYmXwFZDFG16lsxP_SSSENCrawiaoBhO8QDp5iVPcpXGxk6779lzoqIA3zJLlk-_3nHx-jhDK2ZjjOlmNuZY84azQ45ThLWNaZOPdAzI6JB6SEWMZT3Il5RF5EuOKMS4KzR-To5SJIpVKjsi3y6YLZut8Yzv6hl6YypnO-Zb6ms77tWnpp2vX0pltbTCdjXTR4IFwYsrObZFtl3SKsQ_0wpZ2MwSnS9-62MWn5FFtmmif3Z3H5HL69vNknpx_nL2bnJ4npVI6S1JT8JylBW6mteCVUfbKlqpSJTaAl1wJIfPKsNSYotBKCVvyWmSMY1bV2TF5va-76a_Wtiptiz01sAlubcIteOPg70zrvsPSbyEtOOMyxQIv7woE_6O3sYO1i6VtGtNa30fQUuQ6V5zdk0yF-j-ZCXy_ljmSL_4hV74PLf4YaCEyhVZxhPI9VAYfY7D1oT3OYBgKWMHgPQzewzAU8GsoYIfS539-z0H4ewoQeLUHblxjb-9dGBbzBQYoT_Zy9NzuDnITrgHt1RK-fJhBdnZWvP86ncIk-wk76dL8</recordid><startdate>201007</startdate><enddate>201007</enddate><creator>Travers, Jared B.</creator><creator>Berry, Damien</creator><creator>Yao, Yongxue</creator><creator>Yi, Qiaofang</creator><creator>Konger, Raymond L.</creator><creator>Travers, Jeffrey B.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>4T-</scope><scope>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201007</creationdate><title>Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists</title><author>Travers, Jared B. ; Berry, Damien ; Yao, Yongxue ; Yi, Qiaofang ; Konger, Raymond L. ; Travers, Jeffrey B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6673-2a91802980207741da6ebec6d6c031020164458da02aa997664ec1f43011026f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Dose-Response Relationship, Radiation</topic><topic>Experiments</topic><topic>Free radicals</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lipids</topic><topic>Mass spectrometry</topic><topic>Oxidative Stress</topic><topic>Phosphorylcholine - antagonists & inhibitors</topic><topic>Phosphorylcholine - metabolism</topic><topic>Phosphorylcholine - pharmacology</topic><topic>Platelet Membrane Glycoproteins - agonists</topic><topic>Proteins</topic><topic>Quinazolines - pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Rodents</topic><topic>Skin - metabolism</topic><topic>Skin - radiation effects</topic><topic>Time Factors</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Travers, Jared B.</creatorcontrib><creatorcontrib>Berry, Damien</creatorcontrib><creatorcontrib>Yao, Yongxue</creatorcontrib><creatorcontrib>Yi, Qiaofang</creatorcontrib><creatorcontrib>Konger, Raymond L.</creatorcontrib><creatorcontrib>Travers, Jeffrey B.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Docstoc</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Photochemistry and photobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Travers, Jared B.</au><au>Berry, Damien</au><au>Yao, Yongxue</au><au>Yi, Qiaofang</au><au>Konger, Raymond L.</au><au>Travers, Jeffrey B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists</atitle><jtitle>Photochemistry and photobiology</jtitle><addtitle>Photochem Photobiol</addtitle><date>2010-07</date><risdate>2010</risdate><volume>86</volume><issue>4</issue><spage>949</spage><epage>954</epage><pages>949-954</pages><issn>0031-8655</issn><eissn>1751-1097</eissn><coden>PHCBAP</coden><abstract>Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production. In addition to cytokines, such as tumor necrosis factor‐alpha (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous in vitro studies in keratinocytes or epithelial cell lines have demonstrated that UVB‐mediated production of PAF agonists is due primarily to the pro‐oxidative effects of this stimulant, resulting in the nonenzymatic production of modified phosphocholines (oxidized glycerophosphocholines). The current studies use human skin to assess whether UVB irradiation generates PAF‐receptor agonists, and the role of oxidative stress in their production. These studies demonstrate that UVB irradiation of human skin results in PAF agonists, which are blocked by the antioxidant vitamin C and the epidermal growth factor receptor inhibitor PD168393. 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subjects | Antioxidants - pharmacology Apoptosis Ascorbic Acid - pharmacology Dose-Response Relationship, Radiation Experiments Free radicals Humans Kinases Lipids Mass spectrometry Oxidative Stress Phosphorylcholine - antagonists & inhibitors Phosphorylcholine - metabolism Phosphorylcholine - pharmacology Platelet Membrane Glycoproteins - agonists Proteins Quinazolines - pharmacology Reactive Oxygen Species - metabolism Receptors, G-Protein-Coupled - agonists Rodents Skin - metabolism Skin - radiation effects Time Factors Ultraviolet Rays |
title | Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists |
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