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增加中白素-36β的表达促进了日本无氧性皮肤炎的血管生成

Reo Komaki¹, Tomomitsu Miyagaki¹, Miho Tanaka¹

¹Department of Dermatology, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan.

International journal of molecular sciences

|July 14, 2023

概括

干白素-36β (IL-36β) 在亚托皮炎 (AD) 皮肤中升高,促进新的血管生长. 这表明IL-36β是治疗AD的潜在治疗点.

科学领域:

免疫皮肤学免疫皮肤学
分子生物学分子生物学
血管新生研究研究

背景情况:

亚托皮炎 (AD) 传统上被视为一个以T助手2 (Th2) 为中心的炎症状况.
新出现的证据表明,其他炎症性细胞因子,包括IL-36家族成员,有助于AD的发病.
虽然IL-36α和IL-36γ已在阿尔茨海默病中得到研究,但IL-36β的作用在很大程度上仍未被探索.

研究的目的:

为了研究介素-36β (IL-36β) 在亚托皮性皮炎 (AD) 中的表达和功能.
确定IL-36β在AD损伤皮肤中的血管生成中的潜在作用.
评估IL-36β作为阿尔茨海默病的潜在治疗点.

主要方法:

对阿尔茨海默病患者和健康对照患者病变皮肤中的IL-36β表达的分析.
在体外研究中使用HaCaT角质细胞来评估IL-36β功能.
研究了下游的信号通路,包括细胞外信号调节激酶1和2 (ERK1/2) 酸化.
量化了血管内皮生长因子A (VEGF-A) 和胎盘生长因子 (PlGF) 的mRNA表达.
在AD皮肤中与皮肤血管密度相关的IL-36β表达.

主要成果:

与健康皮肤相比,在AD损伤皮肤的表皮角质细胞中,IL-36β表达显著增加.
刺激IL-36β促进了通过ERK1/2酸化在HaCaT细胞中的血管内皮生长因子A (VEGF-A) 的产生.
此外,IL-36β还提高了胎盘生长因子 (PlGF) 在角质细胞中的mRNA表达的调节.
角质细胞中IL-36β水平升高与AD皮肤中的皮肤血管数量呈正相关性.

结论:

在阿托皮性皮肤炎患者的皮肤中,IL-36β的调节升高.
IL-36β促进关键的亲血管性因素,这表明它在AD病变中的新血管化中起着作用.
IL-36β代表了一种潜在的新型治疗点,用于控制亚托皮炎中的血管生成.

关键词:

亚洲人口亚洲人口对于IL-36β来说,这是一个很好的方法.血管新生是因为血管新生.亚托邦性皮肤炎的发生.血管内皮生长因子A

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