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PPP3CC gene: a putative modulator of antidepressant response through the B-cell receptor signaling pathway

The Pharmacogenomics Journal volume 14, pages 463–472 (2014)Cite this article

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Abstract

Antidepressant pharmacogenetics represents a stimulating, but often discouraging field. The present study proposes a combination of several methodologies across three independent samples. Genes belonging to monoamine, neuroplasticity, circadian rhythm and transcription factor pathways were investigated in two samples (n=369 and 88) with diagnosis of major depression who were treated with antidepressants. Phenotypes were response, remission and treatment-resistant depression. Logistic regression including appropriate covariates was performed. Genes associated with outcomes were investigated in the STAR*D (Sequenced Treatment Alternatives to Relieve Depression) genome-wide study (n=1861). Top genes were further studied through a pathway analysis. In both original samples, markers associated with outcomes were concentrated in the PPP3CC gene. Other interesting findings were particularly in the HTR2A gene in one original sample and the STAR*D. The B-cell receptor signaling pathway proved to be the putative mediator of PPP3CC’s effect on antidepressant response (P=0.03). Among innovative candidates, PPP3CC, involved in the regulation of immune system and synaptic plasticity, seems promising for further investigation.

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Acknowledgements

Data and biomaterials were obtained from the limited-access data sets distributed from the NIH-supported ‘Sequenced Treatment Alternatives to Relieve Depression' (STAR*D). STAR*D focused on non-psychotic major depressive disorder in adults seen in outpatient settings. The primary purpose of this research study was to determine which treatments work best if the first treatment with medication does not produce an acceptable response This study was supported by NIMH Contract No. N01MH90003 to the University of Texas Southwestern Medical Center. The ClinicalTrials.gov identifier is NCT00021528. We thank Manuel Mayhaus (University of Saarlandes, Germany) for technical assistance with Sequenom MassArray platform.

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Authors and Affiliations

  1. Department of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy

    C Fabbri, A Marsano, A Drago & A Serretti

  2. Neuroscience Department, Unit of Genetics of Neurodegenerative Disorders, IRCCS - Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy

    D Albani & A Chierchia

  3. Laboratoire de Psychologie Medicale, Université Libre de Bruxelles and Psy Pluriel, Centre Europeén de Psychologie Medicale, Brussels, Belgium

    R Calati & J Mendlewicz

  4. Department of Biomedical Science and Morphological and Functional Images, University of Messina, Messina, Italy

    C Crisafulli & M Calabrò

  5. IRCCS Centro Neurolesi "Bonino-Pulejo", Messina, Italy

    M Calabrò

  6. Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy

    M Calabrò

  7. Department of Psychiatry and Psychotherapy, Medical University Vienna, Vienna, Austria

    S Kasper & R Lanzenberger

  8. Department of Psychiatry, Sheba Medical Center, Tel Hashomer, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel

    J Zohar & A Juven-Wetzler

  9. Laboratoire de Psychologie Medicale, Universitè Libre de Bruxelles and Psy Pluriel, Centre Européen de Psychologie Medicale, Brussels, Belgium

    D Souery

  10. School of Medicine, Imperial College, London, UK

    S Montgomery

  11. IRCCS Centro S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy

    A Serretti

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Dr Serretti is or has been a consultant/speaker for Abbott, Astra Zeneca, Clinical Data, Boheringer, Bristol Myers Squibb, Eli Lilly, GlaxoSmithKline, Janssen, Lundbeck, Pfizer, Sanofi, and Servier. The other authors declare no conflict of interest.

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Fabbri, C., Marsano, A., Albani, D. et al. PPP3CC gene: a putative modulator of antidepressant response through the B-cell receptor signaling pathway. Pharmacogenomics J 14, 463–472 (2014). https://doi.org/10.1038/tpj.2014.15

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