Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts

Ohnaka, Keizo; Tanabe, Michiharu; Kawate, Hisaya; Nawata, Hajime; Takayanagi, Ryoichi

doi:10.1016/j.bbrc.2005.01.117

Cited by 250 publications

(160 citation statements)

References 22 publications

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“…Their studies, in osteoblastlike cultures, showed that dexamethasone administration resulted in a decrease in b-catenin levels and inhibition of TCF/LEF-mediated transcription. Ohnaka et al (2005) have reported similar results. They found that Wnt3a-stimulated increases in b-catenin in primary cultured human osteoblasts were attenuated by dexamethasone administration.…”

Section: Neurohormone Regulation: Estrogen and Glucocorticoidssupporting

confidence: 61%

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Gould

Manji

2005

Neuropsychopharmacol

338

253

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Section: Neurohormone Regulation: Estrogen and Glucocorticoidssupporting

confidence: 61%

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Gould

Manji

2005

Neuropsychopharmacol

338

253

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“…Dex effects on ␤-catenin levels were recently studied in several tissues and were shown to be dependent on the cellular type and context. Recent data show that GCs suppresses the canonical Wnt signal in cultured human osteoblasts (35), but others have shown that in rat mammary epithelial tumor cells, Dex up-regulates ␤-catenin protein and transcript expression, and induced a membrane, rather than a nuclear, localization of ␤-catenin (36).…”

Section: Discussionmentioning

confidence: 99%

Involvement of β-catenin and unusual behavior of CBP and p300 in glucocorticosteroid signaling in Schwann cells

Fonte

Grenier

Trousson

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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In the nervous system, glucocorticosteroid hormones play a major role during development and adult life. Myelin-forming cells are among the targets of glucocorticosteroids, which have been shown to promote myelination both in the central and peripheral nervous system. Glucocorticosteroid-stimulated gene transcription is mediated by the glucocorticosteroid receptor (GR) that recruits coactivators of the p160 family, forming a docking platform for secondary coactivators, such as cAMP-response element binding protein (CREB)-binding protein (CBP) or its close homologue, p300. Here, we investigated the role of CBP and p300 in mouse Schwann cells (MSC80). We show that, although the CBP͞p300 binding domain of steroid receptor coactivator-1 is crucial for GR transactivation, neither CBP nor p300 enhanced GR transcriptional activation, as shown by overexpression and small interfering RNA (siRNA) knocking-down experiments. Unexpectedly, overexpression of p300, considered as a coactivator of the GR, resulted in inhibition of GR transcriptional activity. Studies with p300 deletion mutants demonstrated that p300-dependent repression is related to its acetyltransferase activity. Functional and pull-down assays showed that ␤-catenin may be the coactivator replacing CBP in the GR transcriptional complex. Our results suggest the formation of a GR-coactivator complex within Schwann cells, indicating that glucocorticosteroids may act by means of unusual partners in the nervous system, and we show a repressive effect of p300 on nuclear receptors.␤-catenin ͉ coactivator ͉ glucocorticosteroid receptor ͉ nervous system

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“…184,185 Administration of dexamethasone has been shown in osteoblast cultures to oppose the downstream effects of GSK-3 inhibition on ␤-catenin and TCF/LEF-mediated transcription. 186,187 If this finding holds true in the brain, it would represent an interesting relationship between the HPA axis and ␤-catenin/GSK-3.…”

Section: Lithium and Glycogen Synthase Kinase-3mentioning

confidence: 95%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

135

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Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

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Glucocorticoid suppresses the canonical Wnt signal in cultured human osteoblasts

Cited by 250 publications

References 22 publications

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Involvement of β-catenin and unusual behavior of CBP and p300 in glucocorticosteroid signaling in Schwann cells

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

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