Kumar Sanjay, Matthews Qiana L, Sims Brian
Department of Pediatrics/Division of Neonatology and Center of Glial Biology in Medicine at the University of Alabama School of Medicine, University of Alabama, Birmingham, AL, United States.
Microbiology Program, Department of Biological Sciences, College of Science, Technology, Engineering and Mathematics, Alabama State University, Montgomery, AL, United States.
Front Cell Dev Biol. 2021 Jan 11;8:563441. doi: 10.3389/fcell.2020.563441. eCollection 2020.
Microglia are important myeloid cells present in the brain parenchyma that serve a surveillance function in the central nervous system. Microglial cell activation results in neuroinflammation that, when prolonged, can disrupt immune homeostasis and neurogenesis. Activated microglia-derived extracellular vesicles (EVs) may be involved in the propagation of inflammatory responses and modulation of cell-to-cell communication. However, a complete understanding of how EVs are regulated by drugs of abuse, such as cocaine, is still lacking.
Cocaine exposure reduced human microglial cell (HMC3) viability, decreased expression of CD63 and dectin-1 in HMC3-derived EVs, and increased expression of the apoptotic marker histone H2A.x in HMC3-derived EVs.
Cocaine impacts HMC3 cell viability and specific EV protein expression, which could disrupt cellular signaling and cell-to-cell communication.
小胶质细胞是存在于脑实质中的重要髓样细胞，在中枢神经系统中发挥监测功能。小胶质细胞激活会导致神经炎症，若炎症持续时间过长，会破坏免疫稳态和神经发生。活化的小胶质细胞衍生的细胞外囊泡（EVs）可能参与炎症反应的传播和细胞间通讯的调节。然而，对于诸如可卡因等滥用药物如何调节细胞外囊泡，仍缺乏全面了解。
可卡因暴露降低了人小胶质细胞（HMC3）的活力，降低了HMC3衍生的细胞外囊泡中CD63和dectin-1的表达，并增加了HMC3衍生的细胞外囊泡中凋亡标志物组蛋白H2A.x的表达。
可卡因影响HMC3细胞活力和特定的细胞外囊泡蛋白表达，这可能会破坏细胞信号传导和细胞间通讯。
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