Proteomic profiling of the neurons in mice with depressive-like behavior induced by corticosterone and the regulation of berberine: pivotal sites of oxidative phosphorylation

Autor: Shilin Yang, Fan Lei, Yu-lin Feng, Lu-Ling He, Qin Gong, Mu-Lan Wang, Ying-Ying Luo, Lijun Du, Xiao-Jin Yan, Hongwei Gao, Jun Li
Rok vydání: 2019
Předmět:
0301 basic medicine
Male
Proteomics
medicine.medical_specialty
endocrine system
Berberine
Cell Survival
Quantitative proteomics
Down-Regulation
Proteomic analysis
Oxidative phosphorylation
Mitochondrion
lcsh:RC346-429
Oxidative Phosphorylation
03 medical and health sciences
Cellular and Molecular Neuroscience
chemistry.chemical_compound
0302 clinical medicine
Glucocorticoid receptor
Neurotrophic factors
Corticosterone
Internal medicine
medicine
Animals
RNA
Messenger
Molecular Biology
lcsh:Neurology. Diseases of the nervous system
Neurons
Behavior
Animal
Proteomic Profiling
Chemistry
Depression
Research
Reproducibility of Results
Mitochondria
Up-Regulation
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Endocrinology
Gene Expression Regulation
Psychopharmacology
030217 neurology & neurosurgery
hormones
hormone substitutes
and hormone antagonists
Zdroj: Molecular Brain
Molecular Brain, Vol 12, Iss 1, Pp 1-14 (2019)
ISSN: 1756-6606
Popis: Chronic corticosterone (CORT) stress is an anxiety and depression inducing factor that involves the dysfunction of glucocorticoid receptor (GR), brain-derived neurotrophic factor (BDNF), and neuronal plasticity. However, the regulation of proteomic profiles in neurons suffering CORT stress is remaining elusive. Thus, the proteomic profiles of mouse neuronal C17.2 stem cells were comprehensively investigated by TMT (tandem mass tag)-labeling quantitative proteomics. The quantitative proteomics conjugated gene ontology analysis revealed the inhibitory effect of CORT on the expression of mitochondrial oxidative phosphorylation-related proteins, which can be antagonized by berberine (BBR) treatment. In addition, animal studies showed that changes in mitochondria by CORT can affect neuropsychiatric activities and disturb the physiological functions of neurons via disordering mitochondrial oxidative phosphorylation. Thus, the mitochondrial energy metabolism can be considered as one of the major mechanism underlying CORT-mediated depression. Since CORT is important for depression after traumatic stress disorder, our study will shed light on the prevention and treatment of depression as well as posttraumatic stress disorder (PTSD).
Databáze: OpenAIRE
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