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S100B is downregulated in the nuclear proteome of schizophrenia corpus callosum

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European Archives of Psychiatry and Clinical Neuroscience Aims and scope Submit manuscript

Abstract

Here we report the downregulation of S100B in the nuclear proteome of the corpus callosum from nine schizophrenia patients compared to seven mentally healthy controls. Our data have been obtained primarily by mass spectrometry and later confirmed by Western blot. This is an intriguing finding coming from a brain region which is essentially composed by white matter, considering the potential role of S100B in the control of oligodendrocyte maturation. This data reinforce the importance of oligodendrocytes in schizophrenia, shedding more light to its pathobiology.

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References

  1. Bernstein HG, Steiner J, Bogerts B (2009) Glial cells in schizophrenia: pathophysiological significance and possible consequences for therapy. Expert Rev Neurother 9:1059–1071

    Article  CAS  PubMed  Google Scholar 

  2. Deloulme JC, Raponi E, Gentil BJ, Bertacchi N, Marks A, Labourdette G, Baudier J (2004) Nuclear expression of S100B in oligodendrocyte progenitor cells correlates with differentiation toward the oligodendroglial lineage and modulates oligodendrocytes maturation. Mol Cell Neurosci 27:453–465

    Article  CAS  PubMed  Google Scholar 

  3. Fitzsimmons J, Kubicki M, Shenton ME (2013) Review of functional and anatomical brain connectivity findings in schizophrenia. Curr Opin Psychiatry 26:172–187

    Article  PubMed  Google Scholar 

  4. Guo S, Kendrick KM, Zhang J, Broome M, Yu R, Liu Z, Feng J (2013) Brain-wide functional inter-hemispheric disconnection is a potential biomarker for schizophrenia and distinguishes it from depression. NeuroImage Clin 2:818–826

    Article  PubMed Central  PubMed  Google Scholar 

  5. Innocenti GM, Ansermet F, Parnas J (2003) Schizophrenia, neurodevelopment and corpus callosum. Mol Psychiatry 8:261–274

    Article  CAS  PubMed  Google Scholar 

  6. Jahn T, Mussgay L (1989) Die statistische Kontrolle moeglicher Medikamenteneinfluesse in experimentalpsychologischen Schizophreniestudien: Ein Vorschlag zur Berechnung von Chlorpromazina aequivalenten. Z Klin Psychol Psychother 18:10

    Google Scholar 

  7. Liu J, Shi Y, Tang J, Guo T, Li X, Yang Y, Chen Q, Zhao X, He G, Feng G, Gu N, Zhu S, Liu H, He L (2005) SNPs and haplotypes in the S100B gene reveal association with schizophrenia. Biochem Biophys Res Commun 328:335–341

    Article  CAS  PubMed  Google Scholar 

  8. Maccarrone G, Rewerts C, Lebar M, Turck CW, Martins-de-Souza D (2013) Proteome profiling of peripheral mononuclear cells from human blood. Proteomics 13:893–897

    Article  CAS  PubMed  Google Scholar 

  9. Meltzer HY, Fatemi SH (1998) Treatment of schizophrenia. In: Schatzberg AF, Nemeroff CB (eds) The American psychiatric text book of psychopharmacology. American Psychiatric Press, Washington, pp 127–135

    Google Scholar 

  10. Mitterauer BJ (2011) Possible role of glia in cognitive impairment in schizophrenia. CNS Neurosci Ther 17:333–344

    Article  PubMed  Google Scholar 

  11. Rotarska-Jagiela A, Schonmeyer R, Oertel V, Haenschel C, Vogeley K, Linden DE (2008) The corpus callosum in schizophrenia-volume and connectivity changes affect specific regions. Neuroimage 39:1522–1532

    Article  PubMed  Google Scholar 

  12. Rothermundt M, Ahn JN, Jorgens S (2009) S100B in schizophrenia: an update. Gen Physiol Biophys 28 Spec No Focus, F76-81

  13. Rothermundt M, Falkai P, Ponath G, Abel S, Burkle H, Diedrich M, Hetzel G, Peters M, Siegmund A, Pedersen A, Maier W, Schramm J, Suslow T, Ohrmann P, Arolt V (2004) Glial cell dysfunction in schizophrenia indicated by increased S100B in the CSF. Mol Psychiatry 9:897–899

    Article  CAS  PubMed  Google Scholar 

  14. Rothermundt M, Peters M, Prehn JH, Arolt V (2003) S100B in brain damage and neurodegeneration. Microsc Res Tech 60:614–632

    Article  CAS  PubMed  Google Scholar 

  15. Schmitt A, Bertsch T, Henning U, Tost H, Klimke A, Henn FA, Falkai P (2005) Increased serum S100B in elderly, chronic schizophrenic patients: negative correlation with deficit symptoms. Schizophr Res 80:305–313

    Article  PubMed  Google Scholar 

  16. Schroeter ML, Abdul-Khaliq H, Krebs M, Diefenbacher A, Blasig IE (2009) Neuron-specific enolase is unaltered whereas S100B is elevated in serum of patients with schizophrenia—original research and meta-analysis. Psychiatry Res 167:66–72

    Article  CAS  PubMed  Google Scholar 

  17. Steiner J, Bernstein HG, Bielau H, Berndt A, Brisch R, Mawrin C, Keilhoff G, Bogerts B (2007) Evidence for a wide extra-astrocytic distribution of S100B in human brain. BMC Neurosci 8:2 (10 pages)

    Article  PubMed Central  PubMed  Google Scholar 

  18. Steiner J, Bernstein HG, Bielau H, Farkas N, Winter J, Dobrowolny H, Brisch R, Gos T, Mawrin C, Myint AM, Bogerts B (2008) S100B-immunopositive glia is elevated in paranoid as compared to residual schizophrenia: a morphometric study. J Psychiatr Res 42:868–876

    Article  PubMed  Google Scholar 

  19. Steiner J, Bielau H, Bernstein HG, Bogerts B, Wunderlich MT (2006) Increased cerebrospinal fluid and serum levels of S100B in first-onset schizophrenia are not related to a degenerative release of glial fibrillar acidic protein, myelin basic protein and neurone-specific enolase from glia or neurones. J Neurol Neurosurg Psychiatry 77:1284–1287

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  20. Steiner J, Walter M, Guest P, Myint AM, Schiltz K, Panteli B, Brauner M, Bernstein HG, Gos T, Herberth M, Schroeter ML, Schwarz MJ, Westphal S, Bahn S, Bogerts B (2010) Elevated S100B levels in schizophrenia are associated with insulin resistance. Mol Psychiatry 15:3–4

    Article  CAS  PubMed  Google Scholar 

  21. Steiner J, Westphal S, Schroeter ML, Schiltz K, Jordan W, Muller UJ, Bernstein HG, Bogerts B, Schmidt RE, Jacobs R (2012) Increased S100B + NK cell counts in acutely ill schizophrenia patients are correlated with the free cortisol index, but not with S100B serum levels. Brain Behav Immun 26:564–567

    Article  CAS  PubMed  Google Scholar 

  22. Streitbürger DP, Arelin K, Kratzsch J, Thiery J, Steiner J, Villringer A, Mueller K, Schroeter ML (2012) Validating serum S100B and neuron-specific enolase as biomarkers for the human brain—a combined serum, gene expression and MRI study. PLoS ONE 7:e43284

    Article  PubMed Central  PubMed  Google Scholar 

  23. Takahashi N, Sakurai T, Davis KL, Buxbaum JD (2011) Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia. Prog Neurobiol 93:13–24

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  24. Uranova NA, Vostrikov VM, Vikhreva OV, Zimina IS, Kolomeets NS, Orlovskaya DD (2007) The role of oligodendrocyte pathology in schizophrenia. Int J Neuropsychopharmacol 10:537–545

    Article  CAS  PubMed  Google Scholar 

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Acknowledgments

Authors thank Ms. Maria Lebar for excellent technical assistance. DMS is funded in Brazil by FAPESP (São Paulo Research Foundation, Grant 2013/08711-3).

Conflict of interest

Authors declare no conflict of interest.

Author information

Author notes

  1. Daniel Martins-de-Souza

    Present address: Laboratory of Neuroproteomics, Department of Biochemistry, Institute of Biology, State University of Campinas (UNICAMP), Campinas, São Paulo, Brazil

Authors and Affiliations

  1. Department of Psychiatry, University of Magdeburg, Magdeburg, Germany

    Johann Steiner & Bernhard Bogerts

  2. Center for Behavioral Brain Sciences, Magdeburg, Germany

    Johann Steiner & Bernhard Bogerts

  3. Department of Psychiatry and Psychotherapy, Ludwig Maximilians University of Munich (LMU), Munich, Germany

    Andrea Schmitt, Peter Falkai & Daniel Martins-de-Souza

  4. Laboratory of Neurosciences (LIM-27), Institute of Psychiatry, University of São Paulo, São Paulo, Brazil

    Andrea Schmitt & Daniel Martins-de-Souza

  5. Max Planck Institute for Cognitive and Human Brain Sciences, Leipzig, Germany

    Matthias L. Schroeter

  6. Clinic for Cognitive Neurology, University Hospital, Leipzig, Germany

    Matthias L. Schroeter

  7. Max Planck Institute of Psychiatry, Munich, Germany

    Christoph W. Turck & Daniel Martins-de-Souza

Authors
  1. Johann Steiner
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  2. Andrea Schmitt
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  3. Matthias L. Schroeter
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  4. Bernhard Bogerts
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  5. Peter Falkai
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  6. Christoph W. Turck
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  7. Daniel Martins-de-Souza
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Corresponding author

Correspondence to Daniel Martins-de-Souza.

Additional information

Johann Steiner and Andrea Schmitt have contributed equally to this work.

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Steiner, J., Schmitt, A., Schroeter, M.L. et al. S100B is downregulated in the nuclear proteome of schizophrenia corpus callosum. Eur Arch Psychiatry Clin Neurosci 264, 311–316 (2014). https://doi.org/10.1007/s00406-014-0490-z

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  • DOI: https://doi.org/10.1007/s00406-014-0490-z

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