title: Proteome alterations of cortex and hippocampus tissues in mice subjected to vitamin A depletion.
abstract: Vitamin A regulates the development and maintenance of the central nervous system. Studies of vitamin A depletion (VAD) and mutations of retinoid receptors in rodents have revealed a dysfunction of motor and cognitive abilities. However, the molecular mechanisms underlying these behavioral changes are not well understood. In this study, VAD mice were examined and abnormal motor behavior related to psychosis symptoms was found. With the use of two-dimensional gel electrophoresis (2-DE), two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) and mass spectrometric (MS) technologies, 44 and 23 altered protein spots were identified in the cortex and hippocampus, respectively, in VAD mice. By Western blot, the up-regulation of mitogen-activated protein kinase 1 (MAPK1) and proteasome subunit beta type 2 (PSMB2) in the cortex and that of dihydropyrimidinase-related protein 2 (DPYSL2) and PSMB2 in the hippocampus were observed in VAD mice. Bioinformatic analysis using DAVID revealed that altered proteins induced by VAD showed significant enrichment of (i) glycolysis, cytoskeleton, mitochondrion and glutamate metabolism in the cortex; and (ii) actin binding, dopamine receptor signaling and transmission of nerve impulse in the hippocampus. The up-regulations of DPYSL2, MAPK1 and PSMB2 may indicate the activated neuronal defensive mechanism in VAD brain regions, which may underlie the VAD-related psychosis behavior.
authors.affiliation: Bio-X Center, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
authors.forename: Ke
authors.initials: K
authors.lastname: Huang
authors.forename: Zhao
authors.initials: Z
authors.lastname: Zhang
authors.forename: Baohu
authors.initials: B
authors.lastname: Ji
authors.forename: Hui
authors.initials: H
authors.lastname: Zhu
authors.forename: Kejun
authors.initials: K
authors.lastname: Zhou
authors.forename: Yang
authors.initials: Y
authors.lastname: Li
authors.forename: Jinglei
authors.initials: J
authors.lastname: Yang
authors.forename: Liya
authors.initials: L
authors.lastname: Sun
authors.forename: Zhiyun
authors.initials: Z
authors.lastname: Wei
authors.forename: Guang
authors.initials: G
authors.lastname: He
authors.forename: Linghan
authors.initials: L
authors.lastname: Gao
authors.forename: Lin
authors.initials: L
authors.lastname: He
authors.forename: Chunling
authors.initials: C
authors.lastname: Wan
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D016291:Dizocilpine Maleate; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008297:Male; D013058:Mass Spectrometry; D051379:Mice; D008810:Mice, Inbred C57BL; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D020543:Proteome / Q000378:metabolism*; D011605:Psychoses, Substance-Induced / Q000378:metabolism; D011618:Psychotic Disorders / Q000378:metabolism; D011954:Receptors, Dopamine / Q000502:physiology; D015398:Signal Transduction; D057825:Two-Dimensional Difference Gel Electrophoresis; D014802:Vitamin A Deficiency / Q000378:metabolism*
chemical_list: D000199:Actins; D036341:Intercellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; D020543:Proteome; D011954:Receptors, Dopamine; C095114:collapsin response mediator protein-2; D018698:Glutamic Acid; D016291:Dizocilpine Maleate; D019950:Mitogen-Activated Protein Kinase 1; C569717:PSMB2 protein, mouse; D046988:Proteasome Endopeptidase Complex