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SPION primes THP1 derived M2 macrophages towards M1-like macrophages

•Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes. Potentially, cellul...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2013-11, Vol.441 (4), p.737-742
Main Authors: Laskar, Amit, Eilertsen, Jonas, Li, Wei, Yuan, Xi-Ming
Format: Article
Language:English
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Summary:•Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes. Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ and high TNF α+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which is a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes, and thus these cells may escape detection by iron-oxide nanoparticles (INPs) in-vivo.
ISSN:0006-291X
1090-2104
1090-2104
DOI:10.1016/j.bbrc.2013.10.115