Decreased VEGFR2 expression and increased phosphorylated Akt1 in the prefrontal cortex of individuals with schizophrenia |
| |
| Affiliation: | 1. Departments of Neuropsychiatry, Fukushima Medical University School of Medicine, 960-1295 Fukushima, Japan;2. Department of Psychiatry, Aizu Medical Center, School of Medicine, Fukushima Medical University, 969-3492 Fukushima, Japan;3. Department of Pathology, Brain Research Institute, Niigata University, 951-8585 Niigata, Japan;4. Department of Pathological Neuroscience, Brain Research Institute, Niigata University, 951-8585 Niigata, Japan;5. Department of Community-based Medical Education/Department of Community-based Medicine, Nagoya City University Graduate School of Medical Science, Japan;6. Choju Medical Institute, Fukushimura Hospital, 441-8124, Aichi, Japan;1. Interdisciplinary Laboratory of Clinical Neurosciences (LINC), Department of Psychiatry, Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil;2. Mood Disorders Psychopharmacology Unit (MDPU), University Health Network, University of Toronto, Toronto, Canada;3. Department of Psychiatry, Clinic for Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany;4. Vila Maria Outpatient Clinic, São Paulo, Brazil;5. Department of Psychiatry, Irmandade da Santa Casa de Misericórdia de São Paulo (ISCMSP), Brazil;6. Medical University of Graz, Department of Psychiatry, Graz, Austria;1. Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California Los Angeles, 635 Charles E Young Drive S #225, Los Angeles, CA, 90095, USA;2. Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, 200 UCLA Medical Plaza #265, Los Angeles, CA, 90095, USA;1. Department of Medicine, Johns Hopkins Medical Institution, Baltimore, MD, USA;2. Department of Cognitive Science, University of Vienna, Austria;1. Department of Psychiatry & Behavioral Sciences, University of Miami Miller School of Medicine/Jackson Health System, 1695 NW 9th Ave, 33136, United States;2. Department of Epidemiology and Health Statistics, Fujian Medical University, 1 Xue Yuan Road University Town, Fujian, 350108, China;3. Department of Health Sciences, University of Miami Miller School of Medicine, 1120 NW 14th St, Miami, FL, 33136, United States |
| |
| Abstract: | The Akt signaling pathway involves various cellular processes and depends on extracellular stimuli. Since Akt signaling participates in cytoprotection, synapse plasticity, axon extension, and neurotransmission in the nervous system, alteration in Akt signaling might be a potential cause of schizophrenia. In this study, we performed multiplex fluorescent bead based immunoassays for members of the Akt signaling pathway in postmortem brains of controls and patients with schizophrenia. Vascular endothelial growth factor receptor 2 (VEGFR2/KDR) was significantly decreased in the prefrontal cortex (PFC) of patients with schizophrenia, and the expression level of VEGFR2 was inversely correlated with the positive symptom subscale of the Diagnostic Instrument for Brain Studies (DIBS) in patients with schizophrenia. There was also an increase in phosphorylated Akt1 in the PFC in the patients, though the ratio of phospho/total Akt1 is not significantly different. In the nucleus accumbens (NAcc) there was no significant difference in expression and phosphorylation levels of Akt signaling proteins. Genetic analysis revealed a significant correlation of a SNP of KDR (rs7692791) with ERK1/2 and Akt1 phospho/total rates. Since VEGFR2 participates in angiogenesis and neurotrophic activation, either or both functions might be responsible for onset of schizophrenia. |
| |
| Keywords: | Akt signaling VEGFR2 Postmortem brain Schizophrenia Multiplex fluorescent bead based immunoassay SNPs |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
