Endocytosis and intracellular processing of platelet microparticles by brain endothelial cells.
Bottom Line: Platelet-derived microparticle uptake was greatly diminished by treatment of HBEC with cytochalasin D, an inhibitor of microfilament formation required for both phagocytosis and macropinocytosis, with methyl-β-cyclodextrin that depletes membrane cholesterol needed for macropinocytosis and with amiloride that inhibits the Na(+)/H(+) exchanger involved in macropinocytosis.In conclusion, PMP are taken up by active endocytosis in HBEC, involving mechanisms consistent with both phagocytosis and macropinocytosis.These findings identify new processes by which PMP could modify endothelial cell phenotype and functions.
Affiliation: Department of Pathology, University of Sydney, Camperdown, Australia. firstname.lastname@example.orgShow MeSH
Related in: MedlinePlus
Mentions: To search for PMP fusion with the endothelial membrane and to detect a possible PMP fragmentation once internalized, PMP content was stained with soluble calcein AM (green) in addition to the membranous PKH26-labelling (red). After staining, 48% of PMP were double labelled for both calcein and PKH26 (Fig. 2A). Figure 2B shows that, after PMP internalization by HBEC, no PKH26 was transferred from PMP to endothelial membrane and no entrapped calcein was released within the cytosol, suggesting that PMP content did not diffuse inside the target cell but remained co-localized with PMP membranes. This observation clearly indicates that PMP internalization by HBEC does not involve the fusion of PMP lipids with the endothelial plasma membrane but, rather, an uptake of PMP material with subsequent localization in intracellular vesicles.
Affiliation: Department of Pathology, University of Sydney, Camperdown, Australia. email@example.com