INT13995

Context Info Confidence 0.74 First Reported 1989 Last Reported 2010 Negated 8 Speculated 2 Reported most in Abstract Documents 96 Total Number 98 Disease Relevance 48.21 Pain Relevance 26.54

pigmentation (gr)

Anatomy Link Frequency neurons 5 brain 4 hippocampus 3 joints 3 pituitary 3 gr (Mus musculus)

Pain Link Frequency Relevance Heat bDMF 152 100.00 antagonist 60 99.96 agonist 40 99.96 Morphine 204 99.82 antidepressant 72 99.80 Hippocampus 151 99.68 Cholecystokinin 5 99.68 Inflammation 820 99.56 chemokine 40 99.52 dexamethasone 506 99.48

Disease Link Frequency Relevance Heat Repression 57 100.00 Neurodegenerative Disease 33 99.96 Stress 646 99.92 Targeted Disruption 126 99.88 Nervous System Injury 11 99.72 Chronic Obstructive Pulmonary Disease 972 99.62 Hepatocellular Cancer 8 99.60 INFLAMMATION 1122 99.56 Apoptosis 339 99.14 Sprains And Strains 159 99.12

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

In both strains, real-time RT-PCR experiments revealed that decreased expression of GR in adolescence and adulthood is, in fact, preceded by increased GR expression during early life stress exposure.

Gene_expression (expression) of GR associated with stress and sprains and strains

1) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 1.19 Pain Relevance 0.16

In contrast to the strain-independent effect of early life stress on GR expression, however, changes in egr-1 expression occurred only in Balb/c mice, and unlike the biphasic developmental changes in GR mRNA expression, egr-1 mRNA was decreased throughout postnatal development.

Gene_expression (expression) of GR associated with stress and sprains and strains

2) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 1.20 Pain Relevance 0.17

However, neither the time of onset nor the mechanism(s) leading to decreased GR expression during postnatal development are known.

Gene_expression (expression) of GR

3) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 0.75 Pain Relevance 0.05

These findings illustrate that the impact of early life stress on gene expression changes is modulated by the genetic background and that the persistent changes in GR and egr-1 expression that arise early during postnatal developmental are reversible by chronic fluoxetine treatment during adolescence and adulthood.

Gene_expression (expression) of GR associated with stress and fluoxetine

4) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 0.79 Pain Relevance 0.20

Thus, in Balb/c mice, changes in GR and egr-1 expression can independently contribute to the phenotypes resulting from early life stress exposure.

Gene_expression (expression) of GR associated with stress

5) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 0.92 Pain Relevance 0.19

In both strains, real-time RT-PCR experiments revealed that decreased expression of GR in adolescence and adulthood is, in fact, preceded by increased GR expression during early life stress exposure.

Gene_expression (expression) of GR associated with stress and sprains and strains

6) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 1.18 Pain Relevance 0.15

Moreover, there was no consistent overlap of anatomic regions affected by decreased GR and egr-1 protein expression.

Gene_expression (expression) of GR in anatomic regions

7) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 0.98 Pain Relevance 0.19

Thus, the early life stress-induced disruption of the normal stress-hyporesponsive period during infancy is accompanied by increased GR expression.

Gene_expression (expression) of GR associated with stress

8) Confidence 0.74 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 1.19 Pain Relevance 0.18

The present study used two inbred strains of mice that differ in their behavioral responsiveness to stress (Balb/c and C57Bl/6), exposed them to an established paradigm of early life stress (infant maternal separation), and measured their expression of frontal cortical and hippocampal GRs and the putative transcriptional activator of the GR gene, early growth response gene (egr)-1, at defined stages of postnatal development.

Gene_expression (expression) of GR gene associated with stress and sprains and strains

9) Confidence 0.58 Published 2010 Journal Dev. Neurosci. Section Abstract Doc Link 20453467 Disease Relevance 1.11 Pain Relevance 0.13

Glucocorticoid receptor-impaired (GR-i) mice, a transgenic model for affective disorders with hypothalamic-pituitary-adrenal (HPA) axis feedback control deficit, were used to assess the antidepressant-like effects of the mixed melatonin receptor agonist/5-HT(2C) receptor antagonist, agomelatine, compared to the selective 5-HT reuptake inhibitor (SSRI), fluoxetine, on hippocampal neurogenesis, GR and BDNF expression and antidepressant-responsive behaviour (tail suspension test, TST).

Gene_expression (expression) of GR in pituitary associated with fluoxetine, targeted disruption, antidepressant, antagonist, affective disorder, agonist, ssri and neurodegenerative disease

10) Confidence 0.54 Published 2010 Journal Int. J. Neuropsychopharmacol. Section Abstract Doc Link 19775499 Disease Relevance 0.45 Pain Relevance 0.66

Fluoxetine decreased glucocorticoid receptor (GR) gene expression in the prefrontal cortex, amygdala, locus coeruleus and dorsal raphé nucleus, and increased locus coeruleus tyrosine hydroxylase and dorsal raphé nucleus tryptophan hydroxylase-2 (TPH2) gene expression.

Gene_expression (expression) of GR in cortex associated with locus ceruleus, amygdala and fluoxetine

11) Confidence 0.50 Published 2010 Journal Eur. J. Neurosci. Section Abstract Doc Link 20374287 Disease Relevance 0.49 Pain Relevance 1.09

The GR was present in neuronal populations with classical neurotransmitters, especially monoamines and glutamate and with various neuropeptides.

Gene_expression (present) of GR in neuronal associated with glutamate, neurotransmitter, neuropeptide and monoamine

12) Confidence 0.48 Published 1994 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 7825905 Disease Relevance 0.23 Pain Relevance 0.27

The GR is found already in the fetal rat and the development of GR mRNA and receptor protein was followed during the pre- and postnatal periods.

Gene_expression (found) of GR

13) Confidence 0.48 Published 1994 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 7825905 Disease Relevance 0.41 Pain Relevance 0.27

The beneficial effect of CpdA required expression of the GR in T cells and was achieved by down regulating LFA-1 and CD44 on peripheral Th cells and by repressing IL-17 production.

Gene_expression (expression) of GR in T cells

14) Confidence 0.47 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2781169 Disease Relevance 0.74 Pain Relevance 0.13

Corticosterone readily passes the blood–brain barrier and the GR is highly expressed throughout the motive circuit and the limbic system (Reul and De Kloet 1985; Fuxe et al. 1985; Harfstrand et al. 1986).

Gene_expression (expressed) of GR in brain associated with limbic system

15) Confidence 0.46 Published 2009 Journal Psychopharmacology (Berl) Section Body Doc Link PMC2687516 Disease Relevance 0 Pain Relevance 0.16

Therefore, GR-mediated gene expression in the striatum may play a role in the chronic effects of morphine and could be involved in the formation of drug-associated behavior.

Gene_expression (expression) of GR-mediated in striatum associated with morphine

16) Confidence 0.43 Published 2007 Journal Genome Biol Section Body Doc Link PMC2394777 Disease Relevance 0.22 Pain Relevance 1.30

Since it is believed that beneficial effects are often mediated by GR transrepression while many side effects rely on GR transactivation, current research aims at identifying novel substances that dissociate these two features.

Gene_expression (transrepression) of GR

17) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2781169 Disease Relevance 0.77 Pain Relevance 0.25

Flow cytometric analysis confirmed our earlier findings in thymocytes showing that GR inactivation compromised Dex-induced cell death in WEHI 7.1 cells while the pro-apoptotic activity of CpdA was unaffected (Fig. 3C,D).

Gene_expression (inactivation) of GR in thymocytes associated with apoptosis, dexamethasone and death

18) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2781169 Disease Relevance 0.92 Pain Relevance 0.20

5 M CpdA did not alter the expression of the bona fide GR target gene glucocorticoid-induced leucin zipper (GILZ) in Tenc cells while treatment with 10?

Gene_expression (expression) of GR

19) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2781169 Disease Relevance 0.75 Pain Relevance 0.42

Therefore we studied GR expression, as well as the serum cortisol levels, in patients with recently diagnosed RA.

Gene_expression (expression) of GR associated with rheumatoid arthritis

20) Confidence 0.38 Published 2002 Journal Clin. Exp. Rheumatol. Section Abstract Doc Link 12175100 Disease Relevance 0.45 Pain Relevance 0.23

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