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首页> 外文期刊>Journal of dermatological science >Hyperpigmentation in human solar lentigo is promoted by heparanase-induced loss of heparan sulfate chains at the dermal-epidermal junction.
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Hyperpigmentation in human solar lentigo is promoted by heparanase-induced loss of heparan sulfate chains at the dermal-epidermal junction.

机译：乙酰肝素酶诱导的真皮-表皮交界处的硫酸乙酰肝素链的丢失促进了人类日惹斑色素的过度色素沉着。

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BACKGROUND: Skin pigmentation induced by ultraviolet B radiation is caused in part by inflammation mediated by cytokines secreted from keratinocytes and fibroblasts in the irradiated area. Heparanase is also activated in the irradiated skin, and this leads to loss of heparan sulfate at the dermal-epidermal junction (DEJ), resulting in uncontrolled diffusion of heparan sulfate-binding cytokines through the DEJ. However, it is not clear whether heparanase-induced loss of heparan sulfate at the DEJ is involved in the pigmentation process in sun-exposed skin. OBJECTIVE: We examined the role of heparan sulfate in the pigmentation process of human pigmented skin and in pigmented skin-equivalent model. METHODS: Heparan sulfate and blood vessels in human pigmented skin, solar lentigo, and non-pigmented skin were evaluated by means of immunohistochemistry. Pigmented skin equivalent models were cultured with or without heparanase inhibitor and the pigmentation levels were compared. RESULTS: In solar lentigo, heparan sulfate was hardly observed, presumably due to the increase of heparanase at the DEJ, in spite of the deposition of core protein of perlecan (also known as heparan sulfate proteoglycan). The number of blood vessels was significantly increased in solar lentigo. In the pigmented skin equivalent model, heparanase inhibitor increased the staining intensity of heparan sulfate at the DEJ and markedly reduced melanogenesis in the epidermis. CONCLUSIONS: Our results indicate that heparanase-induced loss of heparan sulfate at the DEJ is involved in the pigmentation process of human skin. Consequently, heparanase inhibitors can be expected to exert a protective effect against ultraviolet exposure-induced skin pigmentation.
机译：背景：紫外线B辐射诱发的皮肤色素沉着部分是由被照射区域的角质形成细胞和成纤维细胞分泌的细胞因子介导的炎症引起的。乙酰肝素酶在被辐照的皮肤中也被激活，这导致真皮-表皮连接处（DEJ）硫酸乙酰肝素的损失，导致硫酸乙酰肝素结合细胞因子不受控制地扩散通过DEJ。然而，尚不清楚在DEJ照射下乙酰肝素酶诱导的硫酸乙酰肝素损失是否与阳光照射皮肤的色素沉着过程有关。目的：我们研究了硫酸乙酰肝素在人皮肤色素沉着过程和皮肤色素沉着模型中的作用。方法：采用免疫组织化学方法对人色素沉着的皮肤，日晒斑痣和无色素的皮肤中的硫酸乙酰肝素和血管进行评估。在有或没有乙酰肝素酶抑制剂的情况下培养色素沉着的皮肤等效模型，并比较色素沉着水平。结果：在日光性扁豆中，几乎没有观察到硫酸乙酰肝素，这可能是由于DEJ乙酰肝素酶的增加，尽管珍珠白蛋白的核心蛋白（也称为硫酸乙酰肝素蛋白聚糖）已沉积。太阳扁豆的血管数量明显增加。在有色皮肤等效模型中，乙酰肝素酶抑制剂可增加DEJ处硫酸乙酰肝素的染色强度，并显着减少表皮中的黑色素生成。结论：我们的结果表明DEJ中乙酰肝素酶诱导的硫酸乙酰肝素的损失与人类皮肤的色素沉着过程有关。因此，肝素酶抑制剂可望对紫外线照射引起的皮肤色素沉着起到保护作用。

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