Dynamic proteomic analysis of protein expression profiles in whole brain of Balb/c mice subjected to unpredictable chronic mild stress: Implications for depressive disorders and future therapies

Liu, Y; Yang, Nan; Wu, Hao; Zhao, Qing; Ying, Tianyi; Liu, Shangyi; Li, Qing; Liang, Yan; Wang, Tao; Dong, Yilong; Ji, Chao; Zuo, Pingping

doi:10.1016/j.neuint.2011.02.019

Cited by 41 publications

(33 citation statements)

References 56 publications

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“…The CUMS procedure used in the present was previously validated in mice [24], with some modifications. Mice were exposed to social and environmental stressors 2-3 times a day for 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

Chronic Stress Contributes to Cognitive Dysfunction and Hippocampal Metabolic Abnormalities in APP/PS1 Mice

Han

Wang

Geng³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Stress response is determined by the brain, and the brain is a sensitive target for stress. Our previous experiments have confirmed that once the stress response is beyond the tolerable limit of the brain, particularly that of the hippocampus, it will have deleterious effects on hippocampal structure and function; however, the metabolic mechanisms for this are not well understood. Methods: Here, we used morris water maze, elisa and gas chromatography-time of flight/mass spectrometry to observe the changes in cognition, neuropathology and metabolomics in the hippocampus of APP/PS1 mice and wild-type (C57) mice caused by chronic unpredictable mild stress (CUMS), we also further explored the correlation between cognition and metabolomics. Results: We found that 4 weeks of CUMS aggravated cognitive impairment and increased amyloid-β deposition in APP/PS1 mice, but did not affect C57 mice. Under non-stress conditions, compared with C57 mice, there were 8 different metabolites in APP/PS1 mice. However, following CUMS, 3 different metabolites were changed compared with untreated C57 mice. Compared to APP/PS1 mice, there were 7 different metabolites in APP/PS1+CUMS mice. Among these alterations, 3-hydroxybutyric acid, valine, serine, beta-alanine and o-phosphorylethanolamine, which are involved in sphingolipid metabolism, synthesis and degradation of ketone bodies, and amino acid metabolism. Conclusion: The results indicate that APP/PS1 mice are more vulnerable to stress than C57 mice, and the metabolic mechanisms of stress-related cognitive impairment in APP/PS1 mice are related to multiple pathways and networks, including sphingolipid metabolism, synthesis and degradation of ketone bodies, and amino acid metabolism.

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“…The CUMS procedure used in the present was previously validated in mice [24], with some modifications. Mice were exposed to social and environmental stressors 2-3 times a day for 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

Chronic Stress Contributes to Cognitive Dysfunction and Hippocampal Metabolic Abnormalities in APP/PS1 Mice

Han

Wang

Geng³

et al. 2017

Cell Physiol Biochem

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“…The COX I activity assay was carried out with the COX I activity kit (Genmed Scientifics Inc, USA) (32,34,52). Briefly, the mitochondria of cells and tissues were isolated by Dounce tissue grinders as described previously (47,52 …”

Section: Cox I Activity Assaymentioning

confidence: 99%

PGC-1α/ERRα-Sirt3 Pathway Regulates DAergic Neuronal Death by Directly Deacetylating SOD2 and ATP Synthase β

ZhangXuefei

RenXiaoqing

ZHANGQi

et al. 2016

Antioxidants & Redox Signaling

107

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“…Adenylate kinase 1 maintains the balance between ATP consumption and production by catalyzing the reversible phosphotransfer between ADP, ATP and AMP [30]. A literature search indicated that energy metabolism-related proteins were decreased in positively stimulating conditions, while they increased in stressful conditions or mental disorders [31,32,33,34]. In support of our results, two interesting studies showed that a lower level of brain activation was observed in EE animals following an anxiety-inducing task [35,36].…”

Section: Discussionmentioning

confidence: 99%

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

Kang

Choi²,

Kim³

et al. 2016

Dev Neurosci

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Environmental enrichment (EE) is a typical experimental method that promotes levels of novelty and complexity that enhance experience-dependent neuroplasticity and cognitive behavior function in laboratory animals. Early EE is associated with resilience in the face of later-life challenges. Since increased synaptic activity enhances endogenous neuronal antioxidant defenses, we hypothesized that long-term EE beginning at an early stage may alter the levels of oxidative stress. We investigated global protein expression and oxidative stress in hippocampal proteins from rats nurtured for a 6-month EE beginning in the prenatal period. The analysis of protein expression was carried out using 2-dimensional gel electrophoresis with matrix-associated laser desorption ionization time-of-flight mass spectrometry. Proteins with altered expression were involved in energy metabolism (phosphoglycerate mutase 1, α-enolase isoform 1, adenylate kinase 1, and triose phosphate isomerase) and antioxidant enzymes (superoxide dismutase 1, glutathione S-transferase ω type 1, peroxiredoxin 5, DJ-1, and glial maturation factor β). Using Western blot assays, some of the proteins with altered expression and NADPH oxidase 2 were confirmed to be decreased. Further confirmation was demonstrated with attenuated expression of 7,8-dihydro-8-oxo-deoxyguanine, a DNA oxidative stress marker, in the hippocampus of EE group rats. Our data demonstrate that a long-term EE program beginning in the prenatal and early postnatal phase of development modulates energy metabolism and reduced oxidant stress possibly through enhanced synaptic activity. We provide evidence that EE can be developed as a tool to protect the brain from oxidative stress-induced injury.

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Dynamic proteomic analysis of protein expression profiles in whole brain of Balb/c mice subjected to unpredictable chronic mild stress: Implications for depressive disorders and future therapies

Cited by 41 publications

References 56 publications

Chronic Stress Contributes to Cognitive Dysfunction and Hippocampal Metabolic Abnormalities in APP/PS1 Mice

Chronic Stress Contributes to Cognitive Dysfunction and Hippocampal Metabolic Abnormalities in APP/PS1 Mice

PGC-1α/ERRα-Sirt3 Pathway Regulates DAergic Neuronal Death by Directly Deacetylating SOD2 and ATP Synthase β

Alteration of Energy Metabolism and Antioxidative Processing in the Hippocampus of Rats Reared in Long-Term Environmental Enrichment

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