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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Trends Neurosci. 2021 Feb 11;44(6):492–506. doi: 10.1016/j.tins.2021.01.003

Figure 2: Alterations in circulating EVs and miRNAs after SCI may contribute to remote brain inflammation.

Figure 2:

Schematic diagram that summarizes key findings from [46] analyzing SCI-induced changes in circulating plasma EVs. Thoracic contusion SCI in male mice resulted in multifaceted changes in total plasma EVs at 1d post-injury including a decrease in the overall count, an increase in tetraspanin CD81+ EVs, and modifications in CNS-related miRNA cargo associated with proinflammatory stimulation of astrocytes (comparison with in vitro data from [23]). Tetraspanin protein expression primarily increased in cells at the injury site except for a unique decrease in surface CD81 on astrocytes, which may be the source of increased plasma CD81+ EVs. ICV injection of total plasma EVs from 1d SCI animals induced robust inflammatory gene expression in the brain cortex, including increased reactive astrocyte genes. Future investigation (dotted red arrow, left) is required to further test the hypothesis that EVs released by cells directly from the injury site travel through the blood circulation to seed brain inflammation, which may contribute to long-term neurodegeneration and associated cognitive deficits and depressive-like behavior after SCI. Abbreviations: ANTI-IF, anti-inflammatory; ASTRO, astrocyte; ICV, intracerebroventricular; PRO-IF, pro-inflammatory; miRNA, microRNA; T10, thoracic segment 10; TNFα; tumor necrosis factor α.