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金属蛋白酶-1的组织抑制剂与CD74相互作用,促进AKT信号传递,单细胞招募反应和血管光滑肌细胞增殖

Simon Ebert¹, Lan Zang², Noor Ismail¹

¹Department of Vascular Biology, Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilian-University (LMU) Munich, 81377 Munich, Germany.

|July 29, 2023

概括

组织金属蛋白酶-1抑制剂 (TIMP-1) 与CD74结合,激活免疫细胞并促进血管光滑肌肉细胞的增殖. 这种相互作用在血管炎症和动脉样硬化中起作用.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
血管生物学血管生物学

背景情况:

组织金属蛋白酶-1抑制剂 (TIMP-1) 调节矩阵金属蛋白酶 (MMPs).
TIMP-1与CD74相互作用,CD74是巨细胞迁移抑制因子 (MIF) 的受体.
目前尚不清楚TIMP-1-CD74相互作用的生物学作用.

研究的目的:

研究TIMP-1与CD74.4结合的分子机制.
探索TIMP-1-CD74轴激活对免疫细胞和血管细胞的功能后果.
评估TIMP-1-CD74轴在血管炎症和动脉样硬化中的相关性.

主要方法:

在分析中 (序列对齐,蛋白质与蛋白质对接).
生物化学试验 (共定位,免疫沉,内化).
基于细胞的测定 (激酶阵列,迁移,增殖,粘附).
来自人类动脉硬化病变的scRNA-seq数据的分析.

主要成果:

TIMP-1通过与MIF共享的残留物与CD74结合,导致CD74内部化.
在单细胞中,TIMP-1激活AKT和ERK1/2信号通路.
CD74的TIMP-1参与增强了单细胞的招募和VSMC的增殖.
在人类动脉样硬化病变中,TIMP-1和CD74共同表达.

结论:

TIMP-1-CD74轴是一个新的信号通路.
这个轴促进单细胞招募和VSMC增殖,导致血管炎症.
TIMP-1-CD74相互作用代表了动脉样硬化的潜在治疗标.

关键词:

在此基础上,我们进行了atherogenesis.细胞的迁移/粘附.化学物质化学物质是化学物质.细胞因子细胞因子它们的扩散和扩散.血管炎症血管炎症

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