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BAG-1 can modulate the activity of the extracellular signal

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Ӧͨ BAG-1 ת˻ GR ת˹ϰERKźͨ· ERK)źͨ·ķӻƲ 赥λ йѧԺоԺ ص ʦ ؼ The effect of chronic forced swim stress on depressive-like behaviors and hippocampal B-cell CLL/lymphoma 2-associated athanogene-1 expression ѧλרҵ ѧ ժҪ ӦǵΪϰҪء

Ժ BAG-1ıˮƽӰ죬 HPA)񾭿˱ΪӦƣ the aim of the present study was to investigate the possible role of BAG-1 in depressive-like behaviors induced by stress. Chronic forced swim stress was applied to establish animal model of depression. The main results of the study were as follows: 1. Chronic forced swim stress induced animals to suffer depression which is characterized by decreased exploratory activity and anhedonia. 2. Chronic forced swim stress significantly increased plasma levels of corticosterone. 3. Chronic forced swim stress significantly decreased the expression of BAG-1 in the nucleus (NBAG-1) and increased the expression of BAG-1 in the cytoplasm (CBAG-1) of hippocampal neurons without significant changes of BAG-1 in the whole neurons in hippocampus. 4. Chronic forced swim stress significantly decreased the expression of GR in the nucleus of hippocampal neurons (NGR) without significant changes of GR in the cytoplasm and the whole neurons in hippocampus. 5. Chronic forced swim stress significantly increased the levels of P-ERK1 without significant changes of P-ERK2 and ERK1/2 in the hippocampus. 6. Chronic forced swim stress significantly decreased the levels of MKP-1 in the hippocampus. 7. There are significant correlations between the proteins of NBAG-1 as the co-chaperone molecular of glucocorticoid receptor (GR) and then affect the HPA axis negative feedback. In addition NGRҲܹڶ񾭿ؼõϸźŵ׵ڼø(extracellular signal-regulated protein kinase ӢժҪ Activation of the hypothalamic-pituitary-adrenal (HPA) axis and alterations of the neuronal plasticity are hypothesized to be the etiology underlying depressive disorders. Stress is the most important factor in the vulnerability to depression

P-ERK2 ERK1/2ıˮƽӰ죬 2 ǿӾӦѪƤͪŨȣ 3 ǿӾӦ˺ϸ BAG-1 ıˮƽ which plays a critical role in the neuronal plasticities. ThusB ϸ CLL/ܰ21(B-cell CLL/lymphoma 2-associated athanogene-1ܹھ HPAᷴӦԵGR ĹܣӦҪ̽ȤͺͿȱϸBAG-1ıˮƽ 6 ǿӾӦ˺ MKP-1ıˮƽ

7 ϸ BAG-1ϸ BAG-1ϸ GRMKP-1 ıˮƽΪָأϸBAG-1ıˮƽ MKP-1ıˮƽأ decreased GR tanslocation in the nucleus and increased the activity of P-ERK1 protein in hippocampus. These results suggest that chronic forced stress may destroy the function of the HPA axis and neuronal plasticities and finally induce depression via destroying the tanslocation of GR to nucleus and activating the ERK pathway which resulted from the decreased the transloction of BAG-1 to the nucleus. ѧ ҽѧѧ ԴURL [] ר о_Ŵѧо 4 ǿӾӦ˺ϸGR ıˮƽյΪ which lead to damages in neuronal plasticities and finally result in depression. B-cell CLL/lymphoma 2-associated athanogene-1(BAG-1)оǿӾӦģͣ̽ӦΪ BAG-1ص׵Ӱ죬 GR)Ĺ·ӣ CBAG-1 BAG-1)ΪƤʼ(glucocorticoid receptor can regulate the function of GR

Ҫ£ 1 ǿӾӦ¶Ϊ 5 ǿӾӦ˺P-ERK1ıˮƽΪˣԺ GR ϸGR ıˮƽӰ죬 and induces the hyperactivity of the HPA axis and excessive glucocorticoid productionӦµ--(hypothalamic-pituitary-adrenal BAG-1 can modulate the activity of the extracellular signal-regulated protein kinase (ERK) signal pathway HPAṦܺ񾭿ԡ

MKP-1 and some variables of depressive-like behaviors. In conclusion

chronic forced swim stress decreased the expression of NBAG-1

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