Macrophage exosomal miR-30c-2-3p in atherosclerotic plaques aggravates microglial neuroinflammation during large-artery atherosclerotic stroke via TGF-β/SMAD2 pathway.

Autor: Tang, Yue, Dong, Ming-Hao, Pang, Xiao-Wei, Zhang, Hang, Chu, Yun-Hui, Zhou, Luo-Qi, Yang, Sheng, Zhang, Lu-Yang, You, Yun-Fan, Zhu, Li-Fang, Wang, Wei, Qin, Chuan, Tian, Dai-Shi
Předmět:
Zdroj: Journal of Neuroinflammation; 11/8/2024, Vol. 21 Issue 1, p1-17, 17p
Abstrakt: Circulating miR-30c-2-3p has been closely related to vascular diseases, however, its role and underlying mechanisms in ischemic stroke remained unclear. Our study addressed this gap by observing elevated levels of exosomal miR-30c-2-3p in patients with acute ischemic stroke due to large artery atherosclerosis. Further investigation revealed that these exosomal miR-30c-2-3p primarily originated from macrophages within atherosclerotic plaques, exacerbating ischemic stroke by targeting microglia. Exosomes enriched with miR-30c-2-3p increased microglial inflammatory properties in vivo and aggravated neuroinflammation by inhibiting SMAD2. In summary, our findings revealed a novel mechanism whereby macrophage-derived foam cells within atherosclerotic plaques secrete exosomes with high levels of miR-30c-2-3p, thus aggravate brain damage during ischemic stroke, which serves as crucial link between the periphery and brain. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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