Objective To investigate the regulatory mechanism of endothelial-derived microparticles (EMPs) overexpressing microRNA-126 (miR-126) on immune-inflammatory responses following acute myocardial infarction (AMI).

Methods A total of 35 patients with AMI were selected as AMI group, and 35 healthy individuals who underwent physical examinations during the same period were selected as healthy group. Peripheral blood samples were collected from both groups, and clinical data were recorded. Transmission electron microscopy was employed to observe the morphological characteristics of the microparticles. Flow cytometry was used for the quantitative analysis of EMP levels. Real-time fluorescence quantitative polymerase chain reaction was utilized to detect the expression level of miR-126 within EMPs. Enzyme-linked immunosorbent assay was applied to measure the concentrations of adhesion molecules in peripheral blood. Human umbilical vein endothelial cell lines were cultured in vitro, and miR-126 overexpression group, control group and miR-126 inhibition group were established. After isolating microparticles through differential centrifugation, the THP1 monocyte cell line was treated accordingly. The content of miR-126 and the expression levels of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin and E-selectin in monocytes of each group were detected.

Results Electron microscopy observations revealed that the isolated microparticles possessed intact membrane structures with particle sizes ranging from 100 to 400 nm. Compared with the healthy group, the expression of miR-126 in EMPs from AMI patients was decreased, while the levels of VCAM-1, ICAM-1, E-selectin and P-selectin in plasma were increased, with statistically significant differences (P < 0.001). In vitro experiments demonstrated that, compared with the control group, the expression of monocyte adhesion molecules was downregulated in the miR-126 overexpression group and upregulated in the miR-126 inhibition group, with statistically significant differences (P < 0.01).

Conclusion This study preliminarily elucidates that miR-126 carried by EMPs after AMI participates in immune-inflammatory responses by regulating the expression of monocyte adhesion molecules, providing a new direction for inflammation-targeted therapy for AMI.