EGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder
Affiliation
Univ Arizona, Coll Med, Dept Basic Med SciIssue Date
2018-02-05Keywords
immediate early genesearly growth response gene 3 (EGR3)
brain-derived neurotrophic factor (BDNF)
bipolar disorder
neuroplasticity
regulatory network
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FRONTIERS MEDIA SACitation
EGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder 2018, 12 Frontiers in Behavioral NeuroscienceRights
© 2018 Pfaffenseller, Kapczinski, Gallitano and Klamt. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Bipolar disorder (BD) is a severe psychiatric illness with a consistent genetic influence, involving complex interactions between numerous genes and environmental factors. Immediate early genes (IEGs) are activated in the brain in response to environmental stimuli, such as stress. The potential to translate environmental stimuli into long-term changes in brain has led to increased interest in a potential role for these genes influencing risk for psychiatric disorders. Our recent finding using network-based approach has shown that the regulatory unit of early growth response gene 3 (EGR3) of IEGs family was robustly repressed in postmortem prefrontal cortex of BD patients. As a central transcription factor, EGR3 regulates an array of target genes that mediate critical neurobiological processes such as synaptic plasticity, memory and cognition. Considering that EGR3 expression is induced by brain-derived neurotrophic factor (BDNF) that has been consistently related to BD pathophysiology, we suggest a link between BDNF and EGR3 and their potential role in BD. A growing body of data from our group and others has shown that peripheral BDNF levels are reduced during mood episodes and also with illness progression. In this same vein, BDNF has been proposed as an important growth factor in the impaired cellular resilience related to BD. Taken together with the fact that EGR3 regulates the expression of the neurotrophin receptor p75NTR and may also indirectly induce BDNF expression, here we propose a feed-forward gene regulatory network involving EGR3 and BDNF and its potential role in BD.Note
Open access journal.ISSN
1662-5153Version
Final published versionSponsors
Brazilian funds MCTI/CNPq INCT-TM/CAPES/FAPESP [465458/2014-9]; CNPq/MS/DECIT [466989/2014-8]; PRONEX/FAPERGS [16/2551-0000499-4]; NIH [R01 MH097803]Additional Links
http://journal.frontiersin.org/article/10.3389/fnbeh.2018.00015/fullae974a485f413a2113503eed53cd6c53
10.3389/fnbeh.2018.00015
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Except where otherwise noted, this item's license is described as © 2018 Pfaffenseller, Kapczinski, Gallitano and Klamt. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

