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Background: Hyaluronan (HA) has a unique hydration capacity that contributes to firmness and bounciness of the skin. Epidermal HA declines with skin aging, which may lead to clinical signs of aging including skin wrinkles and loss of hydration and elasticity. Recently, we developed a new cosmetic agent 1‐ethyl‐β‐N‐acetylglucosaminide (β‐NAG2), which enhances HA production in cultured human keratinocytes. The aim of this study was to explore antiaging potential of β‐NAG2 in reconstructed human epidermal models and human clinical trial. Materials and methods: The amount of HA in β‐NAG2‐treated epidermal models by topical application was analyzed by enzyme‐linked immunosorbent assay (ELISA)‐like assay. A randomized, double‐blind and placebo‐controlled study was conducted in Japanese females (n = 33) by topically treating each side of the face with a lotion formulated with β‐NAG2 or placebo for 8 weeks. Results: Topically applied β‐NAG2 dose dependently increased HA production in epidermal models. Treatment with β‐NAG2‐formulated lotion significantly improved skin hydration and elasticity and reduced skin wrinkling in crow's foot areas when compared to the placebo formulation. Conclusion: Topically applied β‐NAG2 promoted epidermal HA production in vitro and showed antiwrinkle activity in vivo accompanying the improvement in skin hydration and elasticity. Our study provides a novel strategy for antiwrinkle care through β‐NAG2‐induced epidermal HA production. [ABSTRACT FROM AUTHOR]

Aquaporin 9 (AQP9) is a member of the aquaglyceroporin family that transports glycerol, urea and other small solutes as well as water. Compared to the expression and function in epidermal keratinocytes of AQP3, another aquaglyceroporin, our knowledge of epidermal AQP9 remains elusive. In this study, we investigated the expression of AQP9 in the human epidermis and cultured keratinocytes. Immunofluorescence studies revealed that AQP9 expression is highly restricted to the stratum granulosum of the human epidermis, where occludin is also expressed at the tight junctions. Interestingly, the AQP3 staining decreased sharply below the cell layers in which AQP9 is expressed. In cultured normal human epidermal keratinocytes (NHEK), knock-down of AQP9 expression in the differentiated cells induced by RNA interference reduced glycerol uptake, which was not as pronounced as was the case with AQP3 knock-down cells. In contrast, similar reduction of urea uptake was detected in AQP9 and AQP3 knock-down cells. These findings suggested that AQP9 expression in NHEK facilitates at least the transport of glycerol and urea. Finally, we analyzed the effect of retinoic acid (RA), a potent stimulator of keratinocyte proliferation, on AQP3 and AQP9 mRNA expression in differentiated NHEK. Stimulation with RA at 1 μM for 24 h augmented AQP3 expression and down-regulated AQP9 expression. Collectively, these results indicate that AQP9 expression in epidermal keratinocytes is regulated in a different manner from that of AQP3. [ABSTRACT FROM AUTHOR]