Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression
Abstract
Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved.
Source:
Medical Hypotheses, 2015, 85, 3, 291-294Funding / projects:
- Defining a cluster of molecular biomarkers for improved diagnostics and therapy of mood disorders (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41029)
DOI: 10.1016/j.mehy.2015.05.015
ISSN: 0306-9877; 1532-2777
PubMed: 26052031
WoS: 000360868100011
Scopus: 2-s2.0-84939563269
Institution/Community
VinčaTY - JOUR AU - Jovičić, Milica J. AU - Lukić, Iva AU - Radojčić, Marija AU - Adžić, Miroslav AU - Marić, Nađa P. PY - 2015 UR - https://vinar.vin.bg.ac.rs/handle/123456789/723 AB - Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved. T2 - Medical Hypotheses T1 - Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression VL - 85 IS - 3 SP - 291 EP - 294 DO - 10.1016/j.mehy.2015.05.015 ER -
@article{ author = "Jovičić, Milica J. and Lukić, Iva and Radojčić, Marija and Adžić, Miroslav and Marić, Nađa P.", year = "2015", abstract = "Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved.", journal = "Medical Hypotheses", title = "Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression", volume = "85", number = "3", pages = "291-294", doi = "10.1016/j.mehy.2015.05.015" }
Jovičić, M. J., Lukić, I., Radojčić, M., Adžić, M.,& Marić, N. P.. (2015). Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression. in Medical Hypotheses, 85(3), 291-294. https://doi.org/10.1016/j.mehy.2015.05.015
Jovičić MJ, Lukić I, Radojčić M, Adžić M, Marić NP. Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression. in Medical Hypotheses. 2015;85(3):291-294. doi:10.1016/j.mehy.2015.05.015 .
Jovičić, Milica J., Lukić, Iva, Radojčić, Marija, Adžić, Miroslav, Marić, Nađa P., "Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression" in Medical Hypotheses, 85, no. 3 (2015):291-294, https://doi.org/10.1016/j.mehy.2015.05.015 . .