β-上腺刺激促进了唾液腺上皮细胞中的内质网膜压力依赖的炎症程序
Kalliopi Moustaka1, Athanasios Stergiopoulos1, Roxane Tenta1
1Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
Clinical and experimental immunology
|June 24, 2024
概括
β-上腺刺激会增加唾液细胞中的IL-6,特别是在Sjögren细胞中.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 肖格伦综合征 (SS) 是一种影响唾液腺的自身免疫性疾病.
- 介乐-6 (IL-6) 是一种促炎性细胞因子,与SS病变产生有关.
- 在SS唾液腺功能障碍中,β-上腺体信号传递和内分泌网膜 (ER) 压力的作用尚未完全理解.
研究的目的:
- 研究β-上腺刺激对人类唇部小唾液腺上皮细胞 (LMSGEC) 中IL-6产生的影响.
- 为了确定这种IL-6产生的依赖于内质网膜 (ER) 压力.
- 为了比较SS患者和健康对照细胞中的这些效应.
主要方法:
- 来自SS患者和对照组的初级LMSGEC被培养并用上腺素刺激.
- 使用qPCR和ELISA测量IL-6的表达.
- 评估ER压力标志物 (GRP78/BiP,PERK,ATF4) 和β-上腺素受体 (β-ARs) 通过西斑,qPCR和免疫光.
- 使用传输电子显微镜 (TEM) 检查了ER形态.
- 使用tauroursodeoxycholic acid (TUDCA) 和RNA沉默 (PERK,ATF4) 调节了ER压力.
主要成果:
- 上腺素刺激提高了LMSGEC中IL-6的产生,这种效应取决于β-AR和ER压力.
- 制ER压力通路 (PERK/ATF4) 或改善ER压力可以防止上腺素诱导的IL-6上调.
- 与对照人群相比,SS患者的LMSGEC在上腺刺激时表现出增强和持续的IL-6产生.
- SS-LMSGEC显示内源性上腺激素信号的增加,扩张的ER和升高的ER压力标志物 (GRP78/BiP).
结论:
- β-上腺刺激显著增加了LMSGEC中的IL-6产量,通过PERK/ATF4 ER压力通路进行调解.
- 在SS-LMSGEC中增强的上腺体信号传递和ER压力有助于持续的IL-6分泌.
- 这些发现突出了潜在的机制,将上腺素通路,ER压力和Sjögren综合征的炎症联系在一起.
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