PM2.5 induces alterations in gene expression profile of platelet-derived extracellular vesicles and mediates cardiovascular injury in rats

Platelet-derived extracellular vesicles (P-EVs), as the most abundant vesicles in blood, have been proven to play cardinal roles in cardiovascular injury. RNAs (especially miRNAs) carried by P-EVs can be transferred to the receptor, which plays a critical role in regulating vascular endothelial function. PM2.5 is one of the most well-known risk factors that cause cardiovascular disease. Therefore, the objective of the current study was to explore whether exposure to PM2.5 would alter the gene expression profile of P-EVs, and to further elucidate the role of RNAs (especially miRNAs) carried by P-EVs in cardiovascular injury induced by PM2.5 exposure. P-EVs were isolated from the platelet-rich plasma which was exposed and unexposed to PM2.5, and the differentially expressed target genes were evaluated using whole-transcriptome gene sequencing. Rats were treated with P-EVs under different exposure conditions (a protein concentration of 50 µg/mL) and an equal volume of normal saline. The pathological damage of the thoracic aorta and cardiac tissue was evaluated and the coagulation function of the rats was detected. The differentially expressed genes were shown to be mainly concentrated in inflammation, angiogenesis, and apoptosis-related pathways. Moreover, P-EVs extracted from PM2.5-exposed plasma had the potential to trigger an inflammatory response, impair vascular endothelial function, disrupt the normal coagulation process, and promote a prothrombotic state. Our study indicated that PM2.5 induces cardiovascular injury in rats by interfering with the gene expression of P-EVs. It will provide new targets for studying the mechanism involved in PM2.5-induced cardiovascular injury.