Effects of dexamethasone on microglial activation in vivo: selective downregulation of major histocompatibility complex class II expression in regenerating facial nucleus
References (47)
- et al.
The effects of the anti-glucocorticoid RU 38486 on steroid-mediated suppression of experimental allergic encephalomyelitis (EAE) in the Lewis rat
Life Sci.
(1989) The effect of cortisone treatment and reoperation on reactive changes in the facial nucleus after axotomy
Brain Res.
(1975)- et al.
Microglial cells but not astrocytes undergo mitosis following rat facial nerve axotomy
Neurosci. Lett.
(1988) - et al.
New expression of myelomonocytic antigens by microglia and perivascular cells following lethal motor neuron injury
J. Neuroimmunol.
(1990) - et al.
Gamma interferon-like immunoreactivity in the rat nervous system
Neuroscience
(1990) - et al.
Local enhancement of major histocompatibility complex (MHC) class I and II expression and cell infiltration in experimental allergic encephalomyelitis around axotomized motor neurons
J. Neuroimmunol.
(1989) - et al.
Messenger RNA for glial fibrillary acidic protein is decreased in rat brain following acute and chronic corticosterone treatment
Mol. Brain Res.
(1990) - et al.
Glucocorticoids regulate the concentration of glial fibrillary acidic protein throughout the brain
Brain Res.
(1989) - et al.
Macrophages and microglia in the nervous system
Trends Neurosci.
(1988) - et al.
Production of tumor necrosis factor-alpha by microglia and astrocytes in culture
Brain Res.
(1989)
Peripheral nerve lesion produces increased levels of major histocompatibility complex antigens in the central nervous system
J. Neuroimmunol.
Expression of Ia antigen on perivascular and microglial cells after sublethal and lethal motor neuron injury
Exp. Neurol.
MHC antigen expression on bulk isolated macrophage-microglia from newborn mouse brain: induction of Ia antigen expression by γ-interferon
J. Neuroimmunol.
Phagocytosis and inflammatory stimuli induce GM-CSF mRNA in macrophages through posttranscriptional regulation
Cell
Analysis of cell surfaces by xenogeneic myeloma-hybrid antibodies: differentiation antigens of rat lymphocytes
Cell
Major histocompatibility complex antigen expression on rat microglia following epidural kainic acid lesions
J. Neurosci. Res.
Localization of glucocorticoid receptor mRNA in the male rat brain by in situ hybridization
Dexamethasone-mediated inhibition of human T cell growth factor and γ-interferon messenger RNA
J. Immunol.
Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance
Science
Displacement of synaptic terminals from regenerating motoneurons by microglial cells
Z. Zellforsch.
Characterization of glucocorticoid type II receptors in neuronal and glial cultures from rat brain
J. Neuroendocrinol.
Corticosteroid-mediated immunoregulation in man
Immunol. Rev.
Induction of macrophage Ia antigen expression by rIFN-γ and downregulation by IFN-α/β and dexamethasone are regulated transcriptionally
J. Immunol.
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2020, Drug Discovery TodayCitation Excerpt :Inhibition of GR activity in the same neurons has a neuroprotective effect on neurons of the amygdala by reducing GABA activity, which has the potential to damage these cells but has also been reported to increase anxiety-related behavior and cause overall HPA axis hyperactivation in a rodent model [65,66]. The glial cells are similarly modulated by GR stimulation, which can dictate the health or disease state [67–70]. Evidence indicates that the anti-inflammatory effects of steroids are likewise governed by GR activity and rely on glial cell responses.
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2012, Molecular and Cellular EndocrinologyCitation Excerpt :Microglia cells are able to produce cytokines and neurotrophic factors, thereby modulating the function of astrocytes and neuronal cells. High doses of the synthetic GR-specific glucocorticoids methylprednisolone and dexamethasone were shown to suppress the expression of MHC II on the surface of microglia cells (Boylan et al., 1999; Kiefer and Kreutzberg, 1991). The suppressive effect of these ligands is likely a result of their high concentrations and GR-selectivity.
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