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Quantitative Subcellular Proteomics of the Orbitofrontal Cortex of Schizophrenia Patients.

Proteomics Unit, Department of Biochemistry, Institute of Chemistry , Federal University of Rio de Janeiro , Rio de Janeiro 21941-909 , Brazil. Laboratory of Neuroproteomics, Department of Biochemistry, Institute of Biology , University of Campinas (UNICAMP) , Campinas 13083-970 , Brazil. Experimental Medicine Research Cluster (EMRC) University of Campinas , Campinas 13083-887 , SP , Brazil. Instituto Nacional de Biomarcadores em Neuropsiquiatria (INBION) , Conselho Nacional de Desenvolvimento Cientı́fico e Tecnológico (CNPq) , São Paulo , Brazil. University of Carabobo , Naguanagua , Carabobo 2005 , Venezuela. Laboratory of Proteomics, LADETEC, Institute of Chemistry , Federal University of Rio de Janeiro , Rio de Janeiro 21941-598 , Brazil. Department of Psychiatry and Psychotherapy , Ludwig Maximilian University of Munich (LMU) , 80539 Munich , Germany.

Journal of proteome research. 2019;(12):4240-4253
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Abstract

Schizophrenia is a chronic disease characterized by the impairment of mental functions with a marked social dysfunction. A quantitative proteomic approach using iTRAQ labeling and SRM, applied to the characterization of mitochondria (MIT), crude nuclear fraction (NUC), and cytoplasm (CYT), can allow the observation of dynamic changes in cell compartments providing valuable insights concerning schizophrenia physiopathology. Mass spectrometry analyses of the orbitofrontal cortex from 12 schizophrenia patients and 8 healthy controls identified 655 protein groups in the MIT fraction, 1500 in NUC, and 1591 in CYT. We found 166 groups of proteins dysregulated among all enriched cellular fractions. Through the quantitative proteomic analysis, we detect as the main biological pathways those related to calcium and glutamate imbalance, cell signaling disruption of CREB activation, axon guidance, and proteins involved in the activation of NF-kB signaling along with the increase of complement protein C3. Based on our data analysis, we suggest the activation of NF-kB as a possible pathway that links the deregulation of glutamate, calcium, apoptosis, and the activation of the immune system in schizophrenia patients. All MS data are available in the ProteomeXchange Repository under the identifier PXD015356 and PXD014350.