Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA248913 | ENA |
REPOSITORIES: ENA
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Project description:The serotonergic system and in particular serotonin 1A receptor (5-HT1AR) are critically implicated in major depressive disorder (MDD), although underlying mechanisms remain enigmatic. Here we demonstrated that 5-HT1AR is palmitoylated in human and rodent brains and identified ZDHHC21 as a major palmitoyl-transferase, whose depletion reduced palmitoylation and consequently signaling functions of 5-HT1AR. Two rodent models for depression show reduced brain ZDHHC21 expression in conjunction with attenuated 5-HT1AR palmitoylation. Moreover, selective knock-down of ZDHHC21 in murine forebrain by itself sufficed to provoke depressive symptoms, demonstrating a causal relationship between 5-HT1AR palmitoylation and depression. Regarding the underlying mechanism, we identified the microRNA miR-30e as a negative regulator of Zdhhc21 expression. By analysis of the post-mortem samples from suicide MDD victims we also found ZDHHC21 expression as well as palmitoylation of 5-HT1AR to be specifically reduced within the prefrontal cortex (PFC), a brain area critically involved in the pathogenesis of depressive symptoms. Our study provides evidence for transcriptional downregulation of 5-HT1AR palmitoylation as a central mechanism in the etiology of depression and even suicide, in effect making the restoration of 5-HT1AR palmitoylation a promising clinical strategy for the treatment of major depressive disorder.
2019-07-16 | PXD012736 | Pride
Project description:Major depressive disorder (MDD) is a common disorder and is responsible for considerable disability in global functioning, anorexia, and severer medical comorbidity. Recently, some reports showed the relationship between MDD and the metabolic disorders such as diabetes. We examined gene expression profiles in the mice prefrontal cortex using genome-wide microarray technology, and determined gene expression profiles with and without chronic mild stress(CMS) for 4 weeks which was often used to make models of depression. To analyze the candidate genes involved in not only depression but dysfunction of physiological homeostasis like diabetes, we campared the gene expression levels between with and without CMS, then we isolated 494 genes showing a more than 2-fold increase or a less than 1/2-fold decrease, in addition, we chose the isolated genes transcriptional products of both samples were confirmed clearly. The prefrontal cortex of C57Bl/6 N sea mice with and without CMS. We mixed tatal RNA from 7 mice prefrontal cortex per each.
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Project description:Gene expression profiling of blood cells in patients with major depressive disorder (MDD) has been used to identify potential biomarkers and to address the pathophysiology of MDD. However, whether alteration in gene expression in blood cells are reflected in the brain of the same individual is unclear. Here, we used an animal model of depression to investigate intra-subject correlation of gene expression patterns between the whole blood (WB) and the medial prefrontal cortex (mPFC). Ovariectomized mice exposed to the chronic mild stress were used as an animal model of depression.
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Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
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