Microparticles from apoptotic platelets promote resident macrophage differentiation

摘要: Platelets shed microparticles not only upon activation, but also ageing by an apoptosis-like process (apoptosis-induced platelet microparticles, PMap). While the activation-induced have widely been studied, much is known about (patho)physiological consequences of PMap formation. Flow cytometry and scanning electron microscopy demonstrated that display activated integrins interact to form microparticle aggregates. were chemotactic for monocytic cells, bound these furthermore stimulated cell adhesion spreading on a fibronectin surface. After prolonged incubation, promoted differentiation, inhibited proliferation. Monocyte membrane receptor analysis revealed increased expression levels CD11b (integrin αMβ2), CD14 CD31 (platelet endothelial molecule-1), chemokine receptors CCR5 CXCR4, CCR2. This indicated polarized cells into resident M2 monocytes. Cells treated with actively consumed oxidized low-density lipoprotein (oxLDL), released matrix metalloproteinases hydrogen peroxide. Further confirmation differentiation towards professional phagocytes came from finding (ox)LDL receptors, CD36 CD68, production proinflammatory immunomodulating cytokines In conclusion, interaction has potential. The apoptotic polarize subset, induce phagocytes.