High Glutamate Decreases S100B Secretion by a Mechanism Dependent on the Glutamate Transporter

Tramontina, Francine; Leite, Marina Concli; Gonçalves, Daniela; Tramontina, Ana Carolina; Souza, Daniela Fraga de; Frizzo, Juliana Karl; Nardin, Patrícia; Gottfried, Carmem; Wofchuk, Susana Tchernin; Gonçalves, Carlos‐Alberto

doi:10.1007/s11064-006-9085-z

Cited by 44 publications

(32 citation statements)

References 29 publications

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“…19 The release of S100B is inversely proportional to the Abbreviations: C, control; DSM-IV, Diagnostic and Statistical Manual of Mental Disorders, fourth edition; MDD, major depressive disorder; PMI, post-mortem interval; S, suicide; SMD, suicide with major depression. uptake of glutamate, 20 suggesting that the altered expression of glutamate receptor subunits, transporters and GLUL witnessed here may be part of a larger glial deficit precipitated through multiple mechanisms. The g-1 and g-2 GABA-A receptor subunits (GABRG1 and GABRG2), GLUL and the GABA transporter (SLC6A1) are part of a larger group of genes controlling GABA synthesis, neurotransmission and turnover, many of which are misexpressed to varying degrees in these cortical areas.…”

Section: Discussionmentioning

confidence: 90%

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

et al. 2007

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The prefrontal cortex is believed to play a major role in depression and suicidal behavior through regulation of cognition, memory, recognition of emotion, and anxiety-like states, with numerous post-mortem studies documenting a prefrontal serotonergic dysregulation considered to be characteristic of depressive psychopathology. This study was carried out to detect changes in gene expression associated with both suicide and major depression using oligonucleotide microarrays (Affymetrix HG-U133 chip set) summarizing expression patterns in primarily ventral regions of the prefrontal cortex (BA44, 45, 46 and 47). A total of 37 male subjects were included in this study, of which 24 were suicides (depressed suicides = 16, nondepressed suicides = 8) and 13 were matched controls. All subjects were clinically characterized by means of psychological autopsies using structured interviews. Unique patterns of differential expression were validated in each of the cortical regions evaluated, with group-specific changes highlighting the involvement of several key neurobiological pathways that have been implicated in both suicide and depression. An overrepresentation of factors involved in cell cycle control and cell division (BA44), transcription (BA44 and 47) and myelination (BA46) was seen in gene ontology analysis of differentially expressed genes, which also highlights changes in the expression of genes involved in ATP biosynthesis and utilization across all areas. Gene misexpression in BA46 was most pronounced between the two suicide groups, with many significant genes involved in GABAergic neurotransmission. The pronounced misexpression of genes central to GABAergic signaling and astrocyte/ oligodendrocyte function provides further support for a central glial pathology in depression and suicidal behavior.

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Section: Discussionmentioning

confidence: 90%

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

et al. 2007

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“…In vitro, extracellular S100B and S100A4 promote neurite outgrowth and neuronal survival by acting through the receptor for advanced glycation end products and heparan sulfate proteoglycans, respectively, both of which are present at the cell surface (29). Moreover, extracellular S100B has been shown to modulate long term neuronal synaptic plasticity (30), glutamate uptake of hippocampal astrocytes (31), and inflammation (32) (for review see Ref. 33).…”

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confidence: 99%

S100A16, a Novel Calcium-binding Protein of the EF-hand Superfamily

Sturchler

Cox

Durussel

et al. 2006

Journal of Biological Chemistry

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S100A16 protein is a new and unique member of the EF-hand Ca2؉ -binding proteins. S100 proteins are cell-and tissue-specific and are involved in many intra-and extracellular processes through interacting with specific target proteins. In the central nervous system S100 proteins are implicated in cell proliferation, differentiation, migration, and apoptosis as well as in cognition. S100 proteins became of major interest because of their close association with brain pathologies, for example depression or Alzheimer's disease. Here we report for the first time the purification and biochemical characterization of human and mouse recombinant S100A16 proteins. Flow dialysis revealed that both homodimeric S100A16 proteins bind two Ca 2؉ ions with the C-terminal EF-hand of each subunit, the human protein exhibiting a 2-fold higher affinity. Trp fluorescence variations indicate conformational changes in the orthologous proteins upon Ca 2؉ binding, whereas formation of a hydrophobic patch, implicated in target protein recognition, only occurs in the human S100A16 protein. In situ hybridization analysis and immunohistochemistry revealed a widespread distribution in the mouse brain. Furthermore, S100A16 expression was found to be astrocyte-specific. Finally, we investigated S100A16 intracellular localization in human glioblastoma cells. The protein was found to accumulate within nucleoli and to translocate to the cytoplasm in response to Ca 2؉ stimulation.

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“…Therefore, S100B could improve the recycling of glutamate in schizophrenia. Contrarily, another study has demonstrated that glutamate inhibits the release of S100B from astrocytes 34 . In conclusion, an increased S100B release from astrocytes may arise in schizophrenia patients due to reduced availability of glutamate, as a counterregulatory mechanism.…”

Section: Potential Links Between S100b and The Pathogenesis Of Schizomentioning

confidence: 99%

Os possíveis papéis da S100B na esquizofrenia

Steiner

Bernstein

Bogerts

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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Background: Scientific evidence for increased S100B concentrations in the peripheral blood of acutely ill schizophrenia patients is consistent. In the past, this finding was mainly considered to reflect astroglial or blood-brain barrier dysfunction. Methods: Using Entrez, PubMed was searched for articles published on or before June 15, 2011, including electronic early release publications, in order to determine other potential links between S100B and current hypotheses for schizophrenia. Results: S100B is potentially associated with the dopamine and glutamate hypotheses. Supporting the glial hypothesis, an increased expression of S100B has been detected in cortical astrocytes of paranoid schizophrenia cases, while decreased oligodendrocytic expression has been observed in residual schizophrenia. Recently, the neuroinflammation hypothesis of schizophrenia has gained attention. S100B may act as a cytokine after secretion from glial cells, CD8+ lymphocytes and NK cells, activating monocytes and microglial cells. Moreover, S100B exhibits adipokine-like properties and may be dysregulated in schizophrenia due to disturbances in insulin signaling, leading to the increased release of S100B and free fatty acids from adipose tissue. Discussion: Dysregulation of pathways related to S100B appears to play a role in schizophrenia. However, S100B is expressed in different cell types and is involved in many regulatory processes. Currently, "the most important" mechanism related to schizophrenia cannot be determined.

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High Glutamate Decreases S100B Secretion by a Mechanism Dependent on the Glutamate Transporter

Cited by 44 publications

References 29 publications

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

S100A16, a Novel Calcium-binding Protein of the EF-hand Superfamily

Os possíveis papéis da S100B na esquizofrenia

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