1. ¹Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine, Seoul, Korea
2. ²Department of Anatomy, Inje University College of Medicine, Seoul, Korea
3. ³Department of Life Science and Research Center for Women's Disease, Sookmyung Women's University, Seoul, Korea

Correspondence: Dr Wang Jae Lee, Department of Anatomy, Seoul National University College of Medicine, 28 Yongon-dong Chongno-gu, Seoul 110-799, Korea. E-mail: kinglee@snu.ac.kr

⁴These authors contributed equally to this work

Received 25 November 2005; Revised 1 May 2006; Accepted 9 May 2006; Published online 28 September 2006.

Abstract

It is well known that UVB (290–320 nm) induces inflammation in skin by the transcription and release of cytokines and chemokines from skin keratinocytes. In addition, it is considered that intracellular reactive oxygen species (ROS) plays an important role in UVB-induced inflammatory response in the skin. Therefore, we investigated the effect of vitamin C, a potent antioxidant, on the regulation of UVB-induced skin inflammation via the modulation of chemokines production. Vitamin C uptake into keratinocytes is increased by UVB irradiation in a time- and dose-dependent manner through the translocation of sodium-dependent vitamin C transporter-1 (SVCT-1), a vitamin C-specific transporter, from the cytosol to the membrane. To evaluate the effect of vitamin C on the chemokine mRNA expression, we performed RNase protection assay. As a result, there was a remarkable change in chemokine mRNA expression, especially IL-8 and monocyte chemoattractant protein (MCP)-1 expression. In addition, increased IL-8 and MCP-1 mRNA expressions were suppressed by vitamin C treatment. We also confirmed the results of protein levels measured by ELISA. Taken together, vitamin C uptake is increased in UVB-irradiated keratinocytes through the translocation of SVCT-1 and regulates inflammatory response in the skin via the downregulation of IL-8 and MCP-1 production.