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  • Title: Triolein reduces MMP-1 upregulation in dermal fibroblasts generated by ROS production in UVB-irradiated keratinocytes.
    Author: Leirós GJ, Kusinsky AG, Balañá ME, Hagelin K.
    Journal: J Dermatol Sci; 2017 Feb; 85(2):124-130. PubMed ID: 27932255.
    Abstract:
    BACKGROUND: Cytokine production and oxidative stress generated by ultraviolet radiation B (UVB) skin exposure are main factors of skin photoaging. Interleukin-6 (IL-6) produced by irradiated keratinocytes is proposed to have a role in metalloproteinases (MMPs) expression activation in dermal fibroblasts. OBJECTIVES: We examined the effect of triolein treatment of UVB-irradiated keratinocytes on MMP1 (interstitial collagenase) expression response of dermal fibroblasts. We assayed UVB-irradiated keratinocytes soluble signals, mainly IL-6 and reactive oxygen species (ROS). METHODS: IL-6 expression and ROS generation were assayed in UVB-irradiated keratinocytes. MMP1 mRNA expression response was assayed in fibroblasts grown in keratinocytes conditioned medium. We evaluated the effect of treating keratinocytes with triolein on IL-6 expression and ROS generation in keratinocytes, and MMP1 expression in fibroblasts. RESULTS: The irradiation of epidermal cells with sublethal UVB doses increased IL-6 expression and ROS generation. Conditioned culture medium collected from keratinocytes was used to culture dermal fibroblasts. MMP1 mRNA expression increase was observed in fibroblasts cultured in medium collected from UVB-irradiated keratinocytes. Triolein treatment reduced the IL-6 expression and ROS generation in keratinocytes and this effect was reflected in downregulation of MMP1 expression in fibroblasts. CONCLUSIONS: Triolein reduces both the expression of IL-6 and ROS generation in irradiated keratinocytes. It seems to exert an anti-inflammatory and anti-oxidative stress effect on irradiated keratinocytes that in turn reduces MMP1 expression in dermal fibroblasts. Collectively, these results indicate that triolein could act as a photoprotective agent.
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