LAUSR

ABSTRACT Aortic dissection (AD) is the circumferential or transversal tear of the aorta wall that allows blood to infiltrate the layers. MicroRNA (miR) analyses have demonstrated a correlation between miR‐320 family and AD. The underlying mechanism is yet unclear. The matrix metalloproteinases (MMPs) are a group of proteolytic enzymes that could catalyze the degeneration of the extracellular matrix and the destruction of the vasculature. In this study, we investigated whether miR‐320 presented a role in regulating the production of MMPs in aortic dissection. In a cohort of 30 CE patients and 30 healthy controls, the transcription and secretion of MMP‐1, MMP‐2, MMP‐3, MMP‐8, MMP‐9, and MMP‐12 by monocytes were investigated. The monocyte from AD patients presented significantly elevated capacity of MMP expression than those from healthy controls. In contrast, the monocyte/macrophage expression of miR‐320 was significantly lower in AD patients than in controls. In both AD patients and healthy controls, LPS‐activation of macrophages resulted in MMP upregulation and miR‐320 downregulation, in which the MMP expression was significantly higher while the miR‐320 expression was significantly lower in AD patients than in healthy controls. Transfection of miR‐320 mimic did not affect MMP gene transcription but significantly reduced the protein production in some MMPs, demonstrated that miR‐320 were involved in the post‐transcriptional regulation of MMPs. Together, these results demonstrated that miR‐320 could regulate the expression of MMPs by macrophages, through which miR‐320 may interfere with AD development. HIGHLIGHTSWe examined miR‐320 and MMP expression by monocytes/macrophages from AD patients.Macrophages from AD patients presented significantly elevated capacity of MMPs expression.The level of miR‐320 expression was inversely correlated with MMPs expression.Activation of macrophages resulted in MMP upregulation and miR‐320 downregulation.Transfection of miR‐320 mimic reduced the MMPs upregulation in macrophage.