Relationship Between Epidermal Matrix Metalloproteinase-1 and Dermal Collagen Reduction in Skin Subjected to Chronic Sun Exposure.

Background/Objectives: Temporary decreases in dermal collagen caused by artificial ultraviolet exposure are largely affected by increased epidermis-derived matrix metalloproteinase (MMP)-1 levels. However, the role of epidermal MMP-1 in dermal tissue remodeling induced by chronic sun exposure remains unclear. This study aimed to clarify the involvement of epidermal and dermal MMP-1 in dermal collagen reduction induced by chronic sun exposure. Methods: Immunofluorescent staining of 30 facial skin tissue samples was performed to visualize MMP-1. The fluorescence intensity of epidermal MMP-1 observed on microscopic images was analyzed in relation to the severity of dermal tissue remodeling and the dermal collagen fiber density. A similar correlation analysis of the number of dermal MMP-1-positive cells was also performed. Results: Epidermal MMP-1 was observed in the stratum spinosum of skin without severe tissue remodeling; however, in skin with severe dermal tissue remodeling, MMP-1 was localized throughout the epidermis. The epidermal MMP-1 signal area and dermal collagen fiber density were negatively correlated (ρ = -0.383; p = 0.0002; n = 90). However, the ratio of dermal MMP-1-positive cells to total dermal cells was only negatively correlated with the collagen fiber density in skin that was not severely remodeled (ρ = -0.746; p = 0.001; n = 15). Conclusions: Epidermal MMP-1 is involved in the tissue remodeling of skin that is subjected to chronic sun exposure and short-term ultraviolet radiation exposure. However, dermal-cell-derived MMP-1 may be involved in biological processes that require an immediate collagen degradation response. The results of this study demonstrate the importance of controlling epidermal MMP-1 to inhibit dermal tissue remodeling induced by chronic sun exposure and provide new insights that are beneficial to the development of anti-photoaging skincare cosmetics.