Abstract
Myocardial infarction and ischemic stroke are the leading causes of mortality worldwide. Atherosclerosis is their common pathological foundation. It is known that atherosclerosis is characterized by endothelial activation/injury, accumulation of inflammatory immune cells and lipid-rich foam cells, followed by the development of atherosclerotic plaque. Either from arterial vessel wall or blood circulation, endothelial cells, smooth muscle cells, macrophages, T-lymphocytes, B-lymphocytes, foam cells, and platelets have been considered to contribute to the pathogenesis of atherosclerosis. Exosomes, as natural nano-carriers and intercellular messengers, play a significant role in modulation of cell-to-cell communication. Under physiological or pathological conditions, exosomes can deliver their cargos including donor cell-specific proteins, lipids, and nucleic acids to target cells, which in turn affect the function of the target cells. In this review, we will describe the pathophysiological significance of various exosomes derived from different cell types associated with atherosclerosis, and the potential applications of exosome in clinical diagnosis and treatment.
Highlights
According to epidemiological investigation, the number of deaths from atherosclerotic cardiovascular disease (ASCVD) in 2016 was about 2.4 million, accounting for 61% of cardiovascular deaths and 25% of total deaths [1]
The results showed that monocyte exosomes significantly increased monocyte and T lymphocyte infiltration in mouse vascular wall and enhanced plaque formation
The inhibition of caveolin-1 expression by exosomes could be reversed by inhibiting phosphatidylinositol-3-kinase (PI-3-K) or mitogen-induced extracellular kinase 1/2 (MEK1/2). These results suggest the pleiotropic effect of monocyte microparticles on the function of vascular endothelial cells and dissect the related signaling pathways [36]
Summary
Exosomes used to be considered as “extracellular debris” and received little attention. Tang et al demonstrated that exosomes released from LPS-treated macrophages increased the expression of adhesion molecules ICAM-1, chemokine ligand CCL-2 and cytokine IL6 in human vascular endothelial cells, which induced monocyte adhesion and migration [44]. Oil red O staining showed that exosomes secreted by endothelial cell expressing KLF2 significantly reduced atherosclerotic lesions in mice, decreased pro-inflammatory M1 macrophages and increased anti-inflammatory M2 macrophages, which partly resulted from the down-regulation of miR-155 expression [71]. Yao Y et al discovered that exosomes derived from platelets of the atherosclerosis models of ApoE-/- mice exhibited high expression level of miR-25-3p which could target Adam 10 and reduce its expression in the ox-LDL-treated coronary vascular endothelial cells (CVECs), leading to the attenuation of CVEC inflammation [81]. Chrysin could attenuate the expression of miR-92a in exosomes derived from human coronary artery endothelial cell and counteract the inhibitory effect of miR-92a on the expression of KLF2, and play an atheroprotective role [124]
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