각질형성세포에서 자외선에 의해 유도되는 혈청 아밀로이드 A1의 기전
The Mechanism of UV-induced Serum Amyloid A1 in Epidermal Keratinocytes
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Excessive ultraviolet (UV) irradiation on the skin can cause induction of various cytokines, resulting in inflammation of the skin. In addition, repeated UV irradiation leads to increased collagenase which can degrade collagen and cause photoaging in the skin. In the previous study, serum amyloid A(SAA)1 induced and secreted from epidermal keratinocytes by ultraviolet ray acted on dermal fibroblasts, resulting in increases of collagenase and proinflammatory cytokines such as interleukin (IL)-1, IL-6, and IL-8. In this study, experiments were performed to elucidate the mechanism by which serum amyloid A1 is induced by UV irradiation in keratinocytes. Irradiation of keratinocytes with 100 mJ/cm2 of UV resulted in increased SAA1, which was inhibited by pretreatment with NF-κB inhibitor. Next, keratinocytes were treated with proinflammatory cytokines induced by UV irradiation. Among them, IL-1α and IL1β increased the expression of SAA1 the most. Finally, keratinocytes were pretreated with IL-1 inhibitor, followed by irradiation with 100 mJ/cm2 of UV, resulting in suppression of SAA1. In conclusion, UV-induced IL-1α and IL-1β increases SAA1 in epidermal keratinocytes in an autocrine manner. Findings of this study suggest that IL-1 would be the target for anti-photoaging and anti-inflammation in the skin.
Abstract
Excessive ultraviolet (UV) irradiation on the skin can cause induction of various cytokines, resulting in inflammation of the skin. In addition, repeated UV irradiation leads to increased collagenase which can degrade collagen and cause photoaging in the skin. In the previous study, serum amyloid A(SAA)1 induced and secreted from epidermal keratinocytes by ultraviolet ray acted on dermal fibroblasts, resulting in increases of collagenase and proinflammatory cytokines such as interleukin (IL)-1, IL-6, and IL-8. In this study, experiments were performed to elucidate the mechanism by which serum amyloid A1 is induced by UV irradiation in keratinocytes. Irradiation of keratinocytes with 100 mJ/cm2 of UV resulted in increased SAA1, which was inhibited by pretreatment with NF-κB inhibitor. Next, keratinocytes were treated with proinflammatory cytokines induced by UV irradiation. Among them, IL-1α and IL1β increased the expression of SAA1 the most. Finally, keratinocytes were pretreated with IL-1 inhibitor, followed by irradiation with 100 mJ/cm2 of UV, resulting in suppression of SAA1. In conclusion, UV-induced IL-1α and IL-1β increases SAA1 in epidermal keratinocytes in an autocrine manner. Findings of this study suggest that IL-1 would be the target for anti-photoaging and anti-inflammation in the skin.
참고문헌 (11)
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