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- W4313365878 abstract "Abstract Glucocorticoids (GC) are steroid hormones secreted as the end-product of the neuroendocrine stress cascade. Absence or elevated GC mediate neurotoxic responses, suggesting that a narrow window ranging from physiological to slightly high GC mediate protective responses. The beneficial effects are attributed to the transactivation of regulatory proteins and inhibition mediated by glucocorticoid receptor interactions with other cofactors. Elevated GC accelerate beta amyloid (Aβ ) plaque formation and tau phosphorylation, aggregates of which upregulate reactive oxygen species in vulnerable neurons. The oxidative stress negatively regulates glucocorticoid receptor, preventing suppression of the transcriptional factor, nuclear factor-κ B (NF-κ B) by GC. The ensuing inflammatory distress enhance further Aβ accumulation initiating a vicious cycle. The glucocorticoid induced leucine zipper (GILZ) is a gene strongly upregulated by GC and mediates many of the anti-inflammatory and anti-proliferative effects of GC. Mechanistically GILZ inhibits NF-κ B by binding the p65 subunit of NF-κ B in the cytoplasm and thereby prevent transactivation of inflammatory and apoptosis mediators. Although GILZ is constitutively expressed in many tissues including the brain, the expression has been shown to occur with varying dynamics suggesting that the local milieu modulates its expression with consequent effects on cellular responses. Here we investigated the expression profile of GILZ in lipopolysaccharide mediated neuroinflammation model of Alzheimer’s disease. Our data suggest that the GILZ expression is downregulated in neuroinflammation correlating inversely with the pro-inflammatory cytokines and innate immune responses." @default.
- W4313365878 created "2023-01-06" @default.
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- W4313365878 date "2019-05-01" @default.
- W4313365878 modified "2023-09-26" @default.
- W4313365878 title "Glucocorticoid induced leucine zipper is inversely related with neuroinflammation in the brain" @default.
- W4313365878 doi "https://doi.org/10.4049/jimmunol.202.supp.182.54" @default.
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