scholarly journals Urine proteome changes in a chronic unpredictable mild stress (CUMS) mouse model of major depressive disorder

2021 ◽  
pp. 114064
Author(s):  
Yuhang Huan ◽  
Jing Wei ◽  
Tong Su ◽  
Youhe Gao
Keyword(s):  
Major Depressive Disorder ◽  
Mouse Model ◽  
Depressive Disorder ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Urine Proteome ◽  
Proteome Changes

scholarly journals Urine proteome changes in a chronic unpredictable mild stress (CUMS) mouse model of major depressive disorder

2020 ◽  
Author(s):  
Yuhang Huan ◽  
Jing Wei ◽  
Tong Su ◽  
Youhe Gao
Keyword(s):  
Major Depressive Disorder ◽  
Mouse Model ◽  
Depressive Disorder ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Urine Proteome ◽  
Random Combination ◽  
Differential Proteins ◽  
Proteome Changes

AbstractBackgroundMajor depressive disorder (MDD) is a prevalent complex psychiatric disorder with a high prevalence rate. Because MDD is a systemic multifactorial disorder involving complex interactions and disturbances of various molecular pathways, there are no effective biomarkers for clinical diagnosis. Urine is not subjected to homeostatic control, allowing it to reflect the sensitive and comprehensive changes that occur in various diseases. In this study, we examined the urine proteome changes in a CUMS mouse model of MDD.MethodsMale C57BL/6 mice were subjected to chronic unpredictable mild stress for 5 weeks. The tail suspension test (TST) and sucrose consumption test (SCT) were then applied to evaluate depression-like behaviors. The urine proteomes on day 0 and day 36 in the CUMS group were profiled by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS).ResultsA total of 45 differential proteins were identified, 24 of which have been associated with the pathogenic mechanisms of MDD, while 10 proteins have been previously suggested as MDD biomarkers. There was an average of two differential proteins that were identified through 1048574 random combination statistical analyses, indicating that at least 95% of the differential proteins were reliable and not the result of random combination. The differential proteins were mainly associated with blood coagulation, inflammatory responses and central nervous system development.ConclusionsOur preliminary results indicated that the urine proteome can reflect changes associated with MDD in the CUMS model, which provides potential clues for the diagnosis of clinical MDD patients.

A metabolomics-based approach for ranking the depressive level in a chronic unpredictable mild stress rat model

RSC Advances ◽  
2016 ◽  
Vol 6 (31) ◽  
pp. 25751-25765 ◽  
Author(s):  
Xinyu Yu ◽  
Shanlei Qiao ◽  
Di Wang ◽  
Jiayong Dai ◽  
Jun Wang ◽  
...  
Keyword(s):  
Animal Model ◽  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Rat Model ◽  
Untargeted Metabolomics ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Metabolomics Study

An untargeted metabolomics study to investigate the metabolome change in plasma, hippocampus and prefrontal cortex (PFC) in an animal model with a major depressive disorder (MDD) had been conducted.

Peripheral blood mononuclear cell-based metabolomic profiling of a chronic unpredictable mild stress rat model of depression

2014 ◽  
Vol 10 (11) ◽  
pp. 2994-3001 ◽  
Author(s):  
Juan Li ◽  
Ge Tang ◽  
Ke Cheng ◽  
Deyu Yang ◽  
Guanghui Chen ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Peripheral Blood Mononuclear Cell ◽  
Depressive Disorder ◽  
Rat Model ◽  
Peripheral Blood ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Peripheral Blood Mononuclear ◽  
Metabolomic Profiling

Major depressive disorder (MDD) is a debilitating mood disorder with various etiopathological hypotheses.

scholarly journals Molecular mechanism of reward treatment ameliorating chronic stress-induced depressive-like behavior assessed by sequencing miRNA and mRNA in medial prefrontal cortex

2020 ◽  
Author(s):  
Tingting An ◽  
Zhenhua Song ◽  
Jin-Hui Wang
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Molecular Mechanism ◽  
Chronic Stress ◽  
Medial Prefrontal Cortex ◽  
Differentially Expressed ◽  
Mild Stress ◽  
Major Depressive ◽  
Differentially Expressed Mirnas

Abstract Background Major depressive disorder (MDD) is a disease that seriously endangers human health and mental state. Chronic stress and lack of reward may reduce the function of the brain's reward circuits, leading to major depressive disorder. The effect of reward treatment on chronic stress-induced depression-like behaviors and its molecular mechanism in the brain remain unclear.Methods Mice were divided into the groups of control, chronic unpredictable mild stress (CUMS), and CUMS-companion. Mice of CUMS group was performed by CUMS for 4 weeks, and CUMS-companion group was treated by CUMS accompanied with companion. The tests of sucrose preference, Y-maze, and forced swimming were conducted to assess depression-like behaviors or resilience. High-throughput sequencing was used to analyze mRNA and miRNA profiles in the medial prefrontal cortex harvested from control, CUMS-MDD (mice with depression-like behaviors in CUMS group), Reward-MDD (mice with depression-like behaviors in CUMS-companion group), CUMS-resilience (resilient mice in CUMS group), Reward-resilience (resilient mice in CUMS-companion group) mice.Results The results provided evidence that accompanying with companion ameliorated CUMS-induced depression-like behaviors in mice. 45 differentially expressed genes (DEGs) are associated with depression-like behaviors, 8 DEGs are associated with resilience and 59 DEGs are associated with nature reward (companion) were identified. Furthermore, 196 differentially expressed miRNAs were found to be associated with companion. Based on the differentially expressed miRNAs and DEGs data, miRNA-mRNA network was established to be associated with companion.Conclusion Taken together, our data here provided a method to ameliorate depression-like behaviors, and numerous potential drug targets for the prevention or treatment of depression.

scholarly journals Identification of commonly altered genes between in major depressive disorder and a mouse model of depression

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hirotaka Yamagata ◽  
Shusaku Uchida ◽  
Koji Matsuo ◽  
Kenichiro Harada ◽  
Ayumi Kobayashi ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Mouse Model ◽  
Depressive Disorder ◽  
Major Depressive

scholarly journals Transthyretin as a Biomarker to Predict and Monitor Major Depressive Disorder Identified by Whole-Genome Transcriptomic Analysis in Mouse Models

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1124
Author(s):  
Sung-Liang Yu ◽  
Selina Shih-Ting Chu ◽  
Min-Hui Chien ◽  
Po-Hsiu Kuo ◽  
Pan-Chyr Yang ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Hedgehog Signaling ◽  
Stressful Life Events ◽  
Genomic Analysis ◽  
Enrichment Analysis ◽  
Transcriptomic Analysis ◽  
Molecular Networks ◽  
Mild Stress ◽  
Major Depressive

Background: Accumulations of stressful life events result in the onset of major depressive disorder (MDD). Comprehensive genomic analysis is required to elucidate pathophysiological changes and identify applicable biomarkers. Methods: Transcriptomic analysis was performed on different brain parts of a chronic mild stress (CMS)-induced MDD mouse model followed by systemic analysis. QPCR and ELISA were utilized for validation in mice and patients. Results: The highest numbers of genes with significant changes induced by CMS were 505 in the amygdala followed by 272 in the hippocampus (twofold changes; FDR, p < 0.05). Enrichment analysis indicated that the core-enriched genes in CMS-treated mice were positively enriched for IFN-γ response genes in the amygdala, and hedgehog signaling in the hippocampus. Transthyretin (TTR) was severely reduced in CMS-treated mice. In patients with diagnosed MDD, serum concentrations of TTR were reduced by 48.7% compared to controls (p = 0.0102). Paired samples from patients with MDD demonstrated a further 66.3% increase in TTR at remission compared to the acute phase (p = 0.0339). Conclusions: This study provides comprehensive information on molecular networks related to MDD as a basis for further investigation and identifies TTR for MDD monitoring and management. A clinical trial with bigger patient cohort should be conducted to validate this translational study.

scholarly journals Chinese Medicine Formula Kai-Xin-San Ameliorates Neuronal Inflammation of CUMS-Induced Depression-like Mice and Reduces the Expressions of Inflammatory Factors via Inhibiting TLR4/IKK/NF-κB Pathways on BV2 Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Suchen Qu ◽  
Mengqiu Liu ◽  
Cheng Cao ◽  
Chongqi Wei ◽  
Xue-Er Meng ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Chinese Medicine ◽  
Depressive Disorder ◽  
Inflammatory Cytokines ◽  
Scientific Information ◽  
Inflammatory Factors ◽  
Mild Stress ◽  
Major Depressive ◽  
Bv2 Cells ◽  
Pro Inflammatory Cytokines

Kai-Xin-San (KXS) is a traditional Chinese medicinal formula composed of Ginseng Radix et Rhizoma, Polygalae Radix, Acori Tatarinowii Rhizoma, and Poria for relieving major depressive disorder and Alzheimer’s disease in traditional Chinese medicine (TCM) clinics. Previous studies on the antidepressant mechanism of KXS mainly focused on neurotransmitter and neurotrophic factor regulation, but few reports exist on neuronal inflammation regulation. In the current study, we found that KXS exerted antidepressant effects in chronic unpredictable mild stress-induced depression-like mice according to the results of behavioral tests. Meanwhile, KXS also inhibited the activation of microglia and significantly reduced the expression of pro-inflammatory cytokines such as IL-1β, IL−2, and TNF-α in the hippocampus of mice. In mice BV2 microglia cell lines, KXS extract reduced the expression of inflammatory factors in BV2 cells induced by lipopolysaccharide via inhibiting TLR4/IKK/NF-κB pathways, which was also validated by the treatment of signaling pathway inhibitors such as TAK-242 and JSH-23. T0hese data implied that the regulation of pro-inflammatory cytokines in microglia might account for the antidepressant effect of KXS, thereby providing more scientific information for the development of KXS as an alternative therapy for major depressive disorder.

scholarly journals Increased Neuronal DNA/RNA Oxidation in the Frontal Cortex of Mice Subjected to Unpredictable Chronic Mild Stress

2017 ◽  
Vol 1 ◽  
pp. 247054701772474 ◽  
Author(s):  
Alfred M. Maluach ◽  
Keith A. Misquitta ◽  
Thomas D. Prevot ◽  
Corey Fee ◽  
Etienne Sibille ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Frontal Cortex ◽  
Chronic Stress ◽  
Basolateral Amygdala ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Major Depressive ◽  
Unpredictable Chronic Mild Stress ◽  
Rna Oxidation

Background Chronic stress is implicated in the development of various psychiatric illnesses including major depressive disorder. Previous reports suggest that patients with major depressive disorder have increased levels of oxidative stress, including higher levels of DNA/RNA oxidation found in postmortem studies, especially within brain regions responsible for the cognitive and emotional processes disrupted in the disorder. Here, we aimed to investigate whether unpredictable chronic mild stress in mice induces neuronal DNA/RNA oxidation in the prelimbic, infralimbic, and cingulate cortices of the frontal cortex and the basolateral amygdala and to explore potential associations with depressive-like behaviors. We expected that animals subjected to unpredictable chronic mild stress will present higher levels of DNA/RNA oxidation, which will be associated with anxiety-/depressive-like behaviors. Methods C57BL/6J mice were assigned to unpredictable chronic mild stress or nonstress conditions (n = 10/group, 50% females). Following five weeks of unpredictable chronic mild stress exposure, mice were tested in a series of behavioral tests measuring anxiety- and depressive-like behaviors. Frontal cortex and amygdala sections were then immunolabeled for neuronal nuclei, a marker of post-mitotic neurons and anti-8-hydroxy-2-deoxyguanosine/8-oxo-7,8-dihydroguanosine, which reflects both DNA and RNA oxidation. Results Levels of neuronal DNA/RNA oxidation were increased in the frontal cortex of mice subjected to unpredictable chronic mild stress ( p = 0.0207). Levels of neuronal DNA/RNA oxidation in the frontal cortex were positively correlated with z-emotionality scores for latency to feed in the novelty-suppressed feeding test ( p = 0.0031). Statistically significant differences were not detected in basolateral amygdala levels of neuronal DNA/RNA oxidation between nonstress- and unpredictable chronic mild stress-exposed mice, nor were correlations found with behavioral performances for this region. Conclusion Our results demonstrate that unpredictable chronic mild stress induces a significant increase in neuronal DNA/RNA oxidation in the frontal cortex that correlate with behavioral readouts of the stress response. A lack of DNA/RNA oxidation alterations in the basolateral amygdala suggests greater vulnerability of frontal cortex neurons to DNA/RNA oxidation in response to unpredictable chronic mild stress. These findings add support to the hypothesis that chronic stress-induced damage to DNA/RNA may be an additional molecular mechanism underlying cellular dysfunctions associated with chronic stress and present in stress-related disorders.

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