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Glycoxidated ferritin induces the release of microparticles positive for Toll-like receptors derived from peripheral blood CD14+ cells
Both increased serum ferritin levels and Toll-like receptor (TLR) activation show independent association with the inflammatory processes. During inflammation, cell activation and apoptosis are accompanied by the release of membrane-derived microparticles (MPs), which are considered to be mediators...
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Published in: | Archives of biological sciences 2017, Vol.69 (3), p.383-390 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Both increased serum ferritin levels and Toll-like receptor (TLR) activation
show independent association with the inflammatory processes. During
inflammation, cell activation and apoptosis are accompanied by the release of
membrane-derived microparticles (MPs), which are considered to be mediators
of intercellular communication as they induce specific responses in target
cells. The aim of this study was to determine whether glycated and
glycoxidated ferritin induce in vitro release TLR microparticles from CD14+
peripheral blood mononuclear cells. Peripheral blood mononuclear cells were
stimulated with glycated, glycoxidated and native ferritin. The release of
microparticles from CD14+ cells, the presence of TLR2+ and TLR4+ on the
microparticles surface and the presence of interleukins-6 and -8 (IL-6 and
IL-8) inside the microparticles after stimulation were determined by flow
cytometry. The role of nuclear factor ?B (NF-?B) was evaluated by
pretreatment of the cells with the Bay 11-7085 inhibitor. Glycated and
glycoxidated ferritin induced the release of microparticles from CD14+ cells,
the majority of which expressed TLR2+ and TLR4+ on their surface and
contained IL-6 and IL-8. These effects were dependent on NF-?B activation.
Our findings show that glycated and glycoxidated ferritin might be involved
in the release of microparticles and stimulation of inflammatory responses.
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ISSN: | 0354-4664 1821-4339 |
DOI: | 10.2298/ABS160614106L |