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Potential depression and antidepressant-response biomarkers in human lymphoblast cell lines from treatment-responsive and treatment-resistant subjects: roles of SSRIs and omega-3 polyunsaturated fatty acids

Molecular Psychiatry volume 26, pages 2402–2414 (2021)Cite this article

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Abstract

While several therapeutic strategies exist for depression, most antidepressant drugs require several weeks before reaching full biochemical efficacy and remission is not achieved in many patients. Therefore, biomarkers for depression and drug-response would help tailor treatment strategies. This study made use of banked human lymphoblast cell lines (LCLs) from normal and depressed subjects; the latter divided into remitters and non-remitters. Due to the fact that previous studies have shown effects on growth factors, cytokines, and elements of the cAMP-generating system as potential biomarkers for depression and antidepressant action, these were examined in LCLs. Initial gene and protein expression profiles for signaling cascades related to neuroendocrine and inflammatory functions differ among the three groups. Growth factor genes, including VEGFA and BDNF were significantly down-regulated in cells from depressed subjects. In addition, omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been reported to act as both antidepressants and anti-inflammatories, but the mechanisms for these effects are not established. Here we showed that n-3 PUFAs and escitalopram (selective serotonin reuptake inhibitors, SSRIs) treatment increased adenylyl cyclase (AC) and BDNF gene expression in LCLs. These data are consistent with clinical observations showing that n-3 PUFA and SSRI have antidepressant affects, which may be additive. Contrary to observations made in neuronal and glial cells, n-3 PUFA treatment attenuated cAMP accumulation in LCLs. However, while lymphoblasts show paradoxical responses to neurons and glia, patient-derived lymphoblasts appear to carry potential depression biomarkers making them an important tool for studying precision medicine in depressive patients. Furthermore, these data validate usefulness of n-3 PUFAs in treatment for depression.

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Fig. 1: Basal expression levels of genes in LCLs from healthy controls and depressed subjects who responded and did not respond to antidepressant treatment.
Fig. 2: PUFA and escitalopram treatment-altered gene expression in LCLs derived from depressed subjects.
Fig. 3: PUFAs and escitalopram altered G protein and flotillin distribution in LCLs derived from depressed subjects.
Fig. 4: PUFAs and escitalopram decreased cAMP accumulation in LCLs.

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Acknowledgements

The authors are grateful to Athanasia Kotsouris for help with ELISA. This project was supported by NIH Grant R41MH113398 and R01AT009169 and VA grant BX001149. MMR is a VA Career Research Scientist BX004475. PC was also supported by a Science Achievement Scholarship of Thailand (SAST).

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Authors and Affiliations

  1. Department of Physiology, Faculty of Science, Mahidol University, Bangkok, Thailand

    Phatcharee Chukaew & Witchuda Saengsawang

  2. Department of Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL, USA

    Phatcharee Chukaew & Mark M. Rasenick

  3. Department of Psychiatry, University of Illinois College of Medicine, Chicago, IL, USA

    Alex Leow & Mark M. Rasenick

  4. Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, USA

    Alex Leow

  5. Jesse Brown Westside VA Medical Center, Chicago, IL, USA

    Mark M. Rasenick

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MMR has equity in Pax Neuroscience and has received consulting income from Otsuka. He has also received research support from NIH, Lundbeck SA and the Veterans’ Administration. AL has equity in KeyWise AI and is on the scientific advisory board of Buoy Health. The remaining authors declare that they have no conflict of interest.

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Chukaew, P., Leow, A., Saengsawang, W. et al. Potential depression and antidepressant-response biomarkers in human lymphoblast cell lines from treatment-responsive and treatment-resistant subjects: roles of SSRIs and omega-3 polyunsaturated fatty acids. Mol Psychiatry 26, 2402–2414 (2021). https://doi.org/10.1038/s41380-020-0724-6

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