S-Space College of Medicine/School of Medicine (의과대학/대학원) Dermatology (피부과학전공) Journal Papers (저널논문_피부과학전공)
UVB Radiation Induces Apoptosis in Keratinocytes by Activating a Pathway Linked to "BLT2-Reactive Oxygen Species"
Cited 39 time in Web of Science Cited 41 time in Scopus
- Issue Date
- NATURE PUBLISHING GROUP
- JOURNAL OF INVESTIGATIVE DERMATOLOGY; Vol.130(4); 1095-1106
- The 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.
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