1. <italic>MiR-421</italic> mediates PM2.5-induced endothelial dysfunction via crosstalk between bronchial epithelial and endothelial cells.
- Author
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Chen, Yiqing, Zeng, Mengting, Xie, Jinxin, Xiong, Zhihao, Jin, Yuxin, Pan, Zihan, Spanos, Michail, Wang, Tianhui, and Wang, Hongyun
- Abstract
AbstractObjectiveMaterials and methodsResultsConclusionsPM2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM2.5 induced an increased release of
miR-421 from the bronchial epithelium. However, the role ofmiR-421 in PM2.5-induced endothelial injury remains elusive.We utilized a subacute PM2.5-exposure model in micein vivo and an acute injury cell modelin vitro to simulate PM2.5-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role ofmiR-421 in PM2.5-induced endothelial injury.Our findings reveal that inhibition ofmiR-421 attenuated PM2.5-induced endothelial injury and hypertension. Mechanistically,miR-421 inhibited the expression ofangiotensin-converting enzyme 2 (ACE2 ) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule induciblenitric oxide synthase (iNOS) , thereby exacerbating PM2.5-induced endothelial injury.Our results indicate that PM2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cellsvia miR-421 /ACE2 /iNOS signaling pathway, mediating endothelial damage and hypertension.MiR-421 inhibition may offer a new strategy for the prevention and treatment of PM2.5-induced vascular endothelial injury. [ABSTRACT FROM AUTHOR]- Published
- 2024
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