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信号通路调节了巨细胞对脂蛋白聚合物的细胞外消化

Noah Steinfeld¹, Cheng-I J Ma¹, Frederick R Maxfield¹

¹Department of Biochemistry, Weill Cornell Medicine, New York, NY 10065.

Molecular biology of the cell

|November 1, 2023

概括

聚合的LDL会触发巨细胞通过消化外吞和消化这些颗粒. 这一过程涉及释放和PKCα激活,为动脉样硬化提供了新的治疗点.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
心血管研究研究心血管研究

背景情况:

聚合低密度脂蛋白 (agLDL) 与巨细胞的相互作用是动脉样硬化发展的核心.
巨细胞利用消化外来在溶酶体突触中处理agLDL,产生自由胆固醇.

研究的目的:

阐明Syk在调节消化道外中的下游信号通路.
为了确定关键的分子参与者在动脉样硬化期间的agLDL-巨相互作用.

主要方法:

药理抑制和siRNA敲击被用来调查信号通路.
分析布鲁顿氨酸激酶 (BTK),脂酶Cγ2 (PLCγ2), (Ca2+) 的释放,以及蛋白激酶Cα (PKCα) 的激活.

主要成果:

Syk的激活导致了PLCγ2和BTK的激活,这对消化道外至关重要.
通过PLCγ2介导的裂变产生二甲糖醇 (DAG) 和异醇1,4,5-三酸盐 (IP3),导致Ca2+从内分泌网膜 (ER) 释放出来.
DAG和Ca2+都激活了PKCα,这是消化道外食的关键调节者,Ca2+的释放由agLDL上调.

结论:

这项研究详细介绍了一种涉及Syk,PLCγ2,Ca2+释放和PKCα的新型信号级联,该级联涉及agLDL. agLDL的巨消化外.
了解这些机制为缓解动脉样硬化进展提供了潜在的治疗点.

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