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首页> 外文期刊>Journal of dermatological science >A hypothetical mechanism of intraepidermal neurite formation in NC/Nga mice with atopic dermatitis.
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A hypothetical mechanism of intraepidermal neurite formation in NC/Nga mice with atopic dermatitis.

机译：在特应性皮炎的NC / Nga小鼠中表皮内神经突形成的假想机制。

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BACKGROUND: Pruritus is a symptom in atopic dermatitis (AD). Previous studies have reported that increased intraepidermal neurites are observed in AD, suggesting that the neuritogenesis is related to itching in the skin. OBJECTIVE: This study was conducted to reveal the mechanism of intraepidermal neurite formation in AD. METHODS: In this study, we used conventional (Conv) NC/Nga mice with AD. NC/Nga mice maintained in specific pathogen-free (SPF) condition were used as a control with no AD. Distribution of intraepidermal neurites and expression patterns of growth factors (NGF and amphiregulin (AR)) and cell-cell junctional molecules (E-cadherin, zona occludens 1 (ZO-1) and desmoglein 3 (Dsg3)) were examined in the skins by immunohistochemistry or quantitative RT-PCR. Furthermore, detection of gelatinase activity was performed with in situ zymography. The same experiments were conducted in ICR mice for comparison with NC/Nga mice. RESULTS: Neurite density and expression levels of growth factors and gelatinase were remarkably increased in the epidermis of Conv-NC/Nga mice compared with those of SPF-NC/Nga mice. Decreased expression of E-cadherin and ZO-1 and misexpression of Dsg3 were also observed in the atopic skins. In comparison with ICR mice, increases of neurite density and gelatinase activity were found in the skins of SPF-NC/Nga mice but expression levels of growth factors and cell-cell junctional molecules were unchanged. CONCLUSIONS: Increases of growth factors and gelatinase activity may be related to neurite outgrowth in the epidermis of atopic NC/Nga mice. Additionally, abnormal expressions of cell-cell junctional molecules in the epidermis may provide intercellular spaces for the neurite formation.
机译：背景：瘙痒是特应性皮炎（AD）的症状。先前的研究报道，在AD中观察到表皮内神经突增多，这表明神经突发生与皮肤瘙痒有关。目的：本研究旨在揭示AD中表皮神经突形成的机制。方法：在这项研究中，我们使用了传统的（Conv）NC / Nga小鼠AD。保持特定无病原体（SPF）状态的NC / Nga小鼠用作无AD的对照。通过在皮肤上检查皮内神经突的分布和生长因子（NGF和双调蛋白（AR））以及细胞-细胞结合分子（E-钙粘着蛋白，透明带1（ZO-1）和桥粒芯蛋白3（Dsg3））的表达模式。免疫组织化学或定量RT-PCR。此外，用原位酶谱法检测明胶酶活性。在ICR小鼠中进行了相同的实验，以与NC / Nga小鼠进行比较。结果：与SPF-NC / Nga小鼠相比，Conv-NC / Nga小鼠的表皮中神经突密度，生长因子和明胶酶的表达水平显着增加。在特应性皮肤中还观察到E-钙黏着蛋白和ZO-1的表达降低以及Dsg3的错误表达。与ICR小鼠相比，在SPF-NC / Nga小鼠的皮肤中发现了神经突密度和明胶酶活性的增加，但生长因子和细胞-细胞连接分子的表达水平没有变化。结论：生长因子和明胶酶活性的增加可能与特应性NC / Nga小鼠表皮上的神经突生长有关。另外，表皮中细胞-细胞结合分子的异常表达可能为神经突形成提供细胞间空间。

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