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在巨细胞中通过脂肪酸结合蛋白5 (FABP5) 调节的信号通路的蛋白质组分析

Faniya Doswell¹, John D Haley¹, Martin Kaczocha²

¹Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, New York (F.D.); Departments of Anesthesiology (F.D., M.K.) and Pathology (J.D.H.) and Biological Mass Spectrometry Facility, (J.D.H.), Renaissance School of Medicine, Stony Brook University, Stony Brook, New York.

The Journal of pharmacology and experimental therapeutics

|June 7, 2024

概括

巨细胞中的脂肪酸结合蛋白5 (FABP5) 影响炎症反应. 它的缺失改变了路径,揭示了FABP5作为炎症疾病的潜在治疗点.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
生物化学生物化学

背景情况:

慢性炎症与许多疾病有关,巨细胞在协调炎症过程中发挥着中心作用.
巨细胞分化成不同的表型 (M1/M2),每个动员特定的转录程序来决定它们的功能.
脂肪酸结合蛋白5 (FABP5) 是一种在巨细胞中高度表达的脂质伴侣,但其在炎症信号传递中的调节作用仍然不完全理解.

研究的目的:

在M1和M2偏振骨髓衍生巨细胞 (BMDMs) 中通过FABP5调节的信号通路进行系统的分析.
研究FABP5删除对巨细胞蛋白质和蛋白质构成的影响.
确定FABP5在巨细胞炎症信号传递中的新目标和作用.

主要方法:

使用氨基酸稳定同位素标记 (SILAC) 的定量蛋白质和蛋白质分析.
比较M1和M2极化野生类型和FABP5淘汰赛BMDMs.
药理上抑制FABP5,以评估其在托尔类受体2 (TLR2) 信号传递中的作用.

主要成果:

在M1和M2极化BMDM中,FABP5删除显著改变了蛋白质和蛋白表达.
受FABP5损失影响的关键途径包括那些涉及炎症,细胞因子产生,氧化应激和激酶活性的途径.
收费类受体2 (TLR2) 被确定为FABP5的新目标,FABP5的抑制抑制了TLR2介导的激活.

结论:

在调节巨细胞极化和炎症反应方面,FABP5起着至关重要的作用.
失去FABP5会影响多个信号通路,包括TLR2信号传递中的新角色.
抑制FABP5为由巨细胞信号失调驱动的炎症性疾病提供了潜在的治疗策略.

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