1. ¹Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea
2. ²Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea
3. ³Institute of Dermatological Science, Seoul National University, Seoul, Korea

Correspondence: Dr Jin Ho Chung, Department of Dermatology, College of Medicine, Seoul National University Hospital, 28 Yongon-dong. Chongno-Gu, Seoul 110-744, Korea. E-mail: jhchung@snu.ac.kr

Received 2 January 2008; Revised 19 June 2008; Accepted 8 July 2008; Published online 21 August 2008.

Abstract

Myeloid differentiation factor 88 (MyD88) is known as an adaptor protein for the Toll-like receptor (TLR) family and participates in signal transduction by binding to the cytoplasmic Toll/IL-1 receptor (TIR) domains of activated TLR. In this study, we demonstrated that expression of MyD88 is increased in photoaged skin compared with intrinsic aged human skin of the same elderly individuals, and that acute UV irradiation increases MyD88 expression in human skin in vivo. To investigate the effects of these high levels of MyD88 in photoaged skin and acutely UV-irradiated skin, human epidermal keratinocytes were infected with adenovirus expressing wild-type (MyD88wt), dominant-positive (MyD88C), and dominant-negative (MyD88N) MyD88 forms. Overexpression of MyD88wt and MyD88C, but not of MyD88N, increased the basal expressions of IL-6 and matrix metalloproteinase-1 (MMP-1) in human epidermal keratinocytes. Moreover, overexpression of MyD88N prevented UV-induced expressions of IL-6 and MMP-1 by inhibiting UV-induced activation of NF-B and activating protein-1. These results suggest that MyD88 is important in IL-6 and MMP-1 expressions in both acutely UV-irradiated skin and in chronically sun-exposed human skin.