Posts Tagged: exosome

Extracellular Vesicles in Metabolic Syndrome

Extracellular Vesicles in Metabolic Syndrome

M. Carmen Martínez, Ramaroson Andriantsitohaina

Extracellular vesicles (EVs) participate in the development of atherosclerotic plaque. EVMP from smooth muscle cells (pink) induce endothelial dysfunction and macrophage infiltration in the vessel wall through the reactive oxygen species (ROS) production and p38 activation in endothelial cells. EVEXO derived from dendritic cells (blue) increase endothelial inflammation by activation of nuclear factor-κB (NF-κB) pathway and increasing expression of proinflammatory molecules, including vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM1), and E-selectin. [Powerpoint File]

Extracellular Vesicles in Metabolic Syndrome

Extracellular Vesicles in Metabolic Syndrome

M. Carmen Martínez, Ramaroson Andriantsitohaina

Effects of extracellular vesicles (EVs) on blood vessel. EVMP from endothelial cells (dark pink) transfer miR-503 to pericytes and subsequently inhibit vascular endothelial growth factor (VEGF) expression, resulting in decreased migration and proliferation. EVEXO from smooth muscle cells (pink) induce downregulation of LC3 II, ATG5, and Beclin-1 expression in endothelial cells. EVEXO from macrophages (green) evoke intercellular adhesion molecule 1 (ICAM1) overexpression in endothelial cells and reduce level of miR-17. Also, macrophage foam cell–derived EVs favor both migration and adhesion of vascular smooth muscle cells by activating ERK (extracellular signal-regulated kinase) and Akt (protein kinase B/AKT) pathways and by transfer integrins β1 and α5 into vascular smooth muscle cells. EVMP from metabolic syndrome (MetS) patients act on smooth muscle cells and induce overexpression of inducible nitric oxide synthase (iNOS) and monocyte chemoattractant molecule (MCP)-1, leading to vascular hyporeactivity. Also, these EVMP directly act on endothelial cells evoking reduced nitric oxide (NO) production, enhanced cytosolic and mitochondrial reactive oxygen species (ROS) production, and unfolding protein response (UPR). All effects of EVMP from MetS patients are mediated by the interaction Fas/FasL. [Powerpoint File]