雌激醇和IL-6之间存在一个积极的反循环,有助于皮肤纤维化
DeAnna Baker Frost1, Alisa Savchenko2, Naoko Takamura3
1Department of Medicine, Division of Rheumatology and Immunology, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 822, MSC 637, Charleston, SC 29425, USA.
International journal of molecular sciences
|July 13, 2024
概括
介乐-6 (IL-6) 驱动皮肤纤维化在全身性硬化症 (SSc),部分通过雌激素 (E2). 这项研究揭示了皮肤中IL-6和E2之间的积极反循环,有助于纤维化.
科学领域:
- 皮肤病学 皮肤病学
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
背景情况:
- 系统性硬化症 (SSc) 涉及皮肤纤维化,并显示女性占主导地位,暗示激素参与.
- 在SSc患者中增加的互白素-6 (IL-6) 和绝经后妇女的高雌激素 (E2) 表明存在荷尔蒙联系.
- 皮肤中的IL-6增加了芳香酶活性,将转化为E2,在纤维化中可能将IL-6和E2联系起来.
研究的目的:
- 调查雌激醇 (E2) 和互白素-6 (IL-6) 之间的相互作用,在系统性硬化症 (SSc) 中导致皮肤纤维化.
- 确定IL-6是否影响人体皮肤纤维细胞和皮肤组织中的E2产生,反之亦然.
主要方法:
- 使用了来自健康捐赠者和SSc患者的初级皮肤纤维细胞和皮肤组织.
- 组织和细胞被IL-6/sIL-6R或E2刺激,并用芳香酶抑制剂 (阿纳斯托) 或雌激素受体抑制剂 (富尔韦斯特兰特) 治疗.
- 测量了纤维菌素 (FN),III型原蛋白A1 (Col IIIA1) 和V型原蛋白A1 (Col VA1) 的水平.
主要成果:
- 刺激IL-6+sIL-6R诱导了健康皮肤纤维细胞和组织中的E2产生.
- 刺激E2诱导皮肤组织和纤维细胞中的IL-6产生.
- 抑制芳酶或雌激素受体显著降低了SSc纤维细胞和IL-6刺激细胞中的纤维素和原蛋白的产生.
结论:
- 介乐-6 (IL-6) 通过雌激醇 (E2) 部分导致系统性硬化 (SSc) 中皮肤纤维化.
- 在人体皮肤中,E2和IL-6之间存在积极的反循环,促进纤维化过程.
- 准这种IL-6/E2轴可能为SSc皮肤纤维化提供治疗策略.
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