Microparticle (MP)

Microparticles (MPs) are subcellular vesicles (0.1–1 μm) shed from the plasma membranes of activated or apoptotic cells, such as platelets, endothelial cells, leukocytes, and erythrocytes, via calcium-dependent cytoskeletal rearrangements and phospholipid translocation.[1][3] They serve as mediators of intercellular communication by transporting bioactive cargos including proteins, lipids, miRNAs, mitochondrial components, receptors, and autoantigens to target cells through fusion, receptor binding, endocytosis, or immune complex formation.[1][2][3] In physiology, MPs contribute to processes like angiogenesis, endothelial repair, and resolution of inflammation (e.g., neutrophil-derived MPs bearing annexin A1 or TGF-β1 suppress macrophage activation).[2][3] Pathologically, they promote pro-inflammatory effects by stimulating cytokine release (e.g., IL-1β, IL-6, TNF-α, IFN type I), endothelial activation, monocyte recruitment, complement deposition, and tissue factor exposure, amplifying thrombosis and vascular damage.[1][2][3][4] MPs are implicated in autoimmune diseases like SLE (where they break tolerance via autoantigen presentation and B-cell activation), cardiovascular conditions (atherothrombosis, endothelial dysfunction), cancer (tumor growth, metastasis, neoangiogenesis), and other inflammatory states including sepsis and IBD.[1][3][4] While primarily biomarkers of cellular stress and disease activity, their pleiotropic roles—pro- or anti-inflammatory depending on parent cell and stimulus—limit direct therapeutic targeting, with no approved drugs modulating MPs specifically.[1][2][3]

Other names

microparticlesmicrovesiclesplasma membrane-derived vesiclescell-derived microparticles