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Iron mediates gene expression in activated microglia
Author(s) -
Connor J. R.,
Cheepsunthorn P.,
Reid J.,
Radov L. A.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.17_3.x
Subject(s) - microglia , neuroinflammation , lipopolysaccharide , trem2 , microbiology and biotechnology , immunology , gene expression , biology , chemistry , inflammation , gene , biochemistry
Microglia have diverse functions within the brain. Activation of microglia has been described in many neurological diseases and these activated microglia may contribute to the disease process. Following brain injury, activated microglia increase the expression of macrophage‐associated antigens and release neuroactive substances, including reactive oxygen and nitrogen molecules, inflammatory cytokines, and neurotoxins. Iron accumulation accompanies activation of microglia including those associated with neuritic plaques in Alzheimer Disease, infarcted brain areas in stroke, and within the vicinity of plaques in Multiple Sclerosis. The question is whether the effect of iron acummulation in microglia is enhances activation or limits function. To address this question, we examined the influence of iron on gene expression in the murine microglia (BV2) cell line during activation with lipopolysaccharide (LPS) using microarray analysis. The combined presence of LPS and iron resulted in the increased expression of an additional 48 genes and decreased expression of 76 genes compared to the LPS alone group. Among the genes that increased expression in the iron plus LPS group where CD38, CD83, caspase 11, IL15, Mip 1a, interferon alpha family, and Ras superfamily of regulatory GTPase. These results suggest that iron can influence the inflammatory response in microglia elicited by LPS and the removal of tissue debris during any reparative processes.