Experimental Dermatology 2014-10-01

The possible involvement of skin dryness on alterations of the dermal matrix.

Mariko Yokota, Kenji Shimizu, Daiki Kyotani, Shoichi Yahagi, Satoru Hashimoto, Hitoshi Masaki

Index: Exp. Dermatol. 23 Suppl 1 , 27-31, (2014)

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Abstract

Moisturization of the skin plays an important role in maintaining skin homeostasis. Although it is understood that skin dryness initiates the formation of fine wrinkles, there are few objective reports to support that understanding. The purpose of this study was to establish an in vitro dry epidermal model using reconstructed human epidermal equivalents (RHEEs) and to elucidate the relationship between skin dryness and alterations of the dermal matrix which is one of the causes for the formation of wrinkles. An in vitro dry epidermal model was prepared by loading a CaCl2 -filled ampoule on the surface of an RHEE. To evaluate whether the in vitro model reproduced the characteristics of in vivo skin dryness, histological studies and biological assays using a protein array were carried out. Histologically, a distinct fluorescence which originated from carbonylated protein was observed in the stratum corneum. In addition, conditioned medium from RHEEs cultured under dry conditions for 24 h revealed the secretion of several proteins, such as IL-1α, IL-1ra, IL-8, MMP-9, VEGF, M-CSF and IGFBP-2 and IGFBP-3, galectin-1, Cys-C, FGF-6, OPG, Glc and TSP4 compared with normal RHEEs. It has been reported that an increase in IL-1α and the accumulation of carbonylated proteins are observed in the intact stratum corneum in the low humidity winter season. Thus, the in vitro dry epidermal model expresses the features of in vivo skin dryness observed in the winter season. Furthermore, the conditioned medium from RHEEs cultured under dry conditions enhanced MMP-1 secretion by normal human dermal fibroblasts. Taken together, we propose the hypothesis that skin dryness contributes to alterations of the dermal matrix through the elevation of MMP-1 secretion. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.