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UVB Radiation Induces Apoptosis in Keratinocytes by Activating a Pathway Linked to "BLT2-Reactive Oxygen Species"

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dc.contributor.authorRyu, Ho-Cheol-
dc.contributor.authorKim, Cheolmin-
dc.contributor.authorKim, Joo-Young-
dc.contributor.authorChung, Jin-Ho-
dc.contributor.authorKim, Jae-Hong-
dc.date.accessioned2012-07-04T02:12:46Z-
dc.date.available2012-07-04T02:12:46Z-
dc.date.issued2010-04-
dc.identifier.citationJOURNAL OF INVESTIGATIVE DERMATOLOGY; Vol.130(4); 1095-1106ko_KR
dc.identifier.issn0022-202X-
dc.identifier.urihttps://hdl.handle.net/10371/78376-
dc.description.abstractThe role of reactive oxygen species (ROS) in UVB-induced apoptosis has been established, but the molecular mechanisms of their production in response to UVB irradiation in keratinocytes are not well understood. In this study, we demonstrate that levels of BLT2, a low-affinity leukotriene B(4) receptor, and its ligands (LTB(4) and 12(S)HETE) are greatly increased by UVB irradiation and are responsible for the UVB-induced ROS generation in human keratinocytes. Blockade of BLT2 with a BLT2-specific antagonist, LY255283, or with siBLT2 attenuated ROS production and apoptotic cell death detected by a number of criteria. Moreover, we found that the NADPH oxidase family protein Nox1 lies downstream of BLT2 and mediates UVB-induced ROS production and apoptosis. Topical treatment of mouse epidermal skin with LY255283 gave significant protection against UVB-induced sunburn-associated apoptotic damage. Finally, when BLT2-overexpressing transgenic mice were irradiated with UVB, we observed more extensive skin apoptosis. Taken together, our results demonstrate that a "BLT2-Nox1``-linked pathway has a crucial role in UVB-induced ROS generation and mediates apoptosis in human keratinocytes.ko_KR
dc.language.isoenko_KR
dc.publisherNATURE PUBLISHING GROUPko_KR
dc.titleUVB Radiation Induces Apoptosis in Keratinocytes by Activating a Pathway Linked to "BLT2-Reactive Oxygen Species"ko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor류호철-
dc.contributor.AlternativeAuthor김철민-
dc.contributor.AlternativeAuthor김주영-
dc.contributor.AlternativeAuthor정진호-
dc.contributor.AlternativeAuthor김재홍-
dc.identifier.doi10.1038/jid.2009.436-
dc.citation.journaltitleJOURNAL OF INVESTIGATIVE DERMATOLOGY-
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