Show simple item record

dc.contributor.authorPfaffenseller, Bianca
dc.contributor.authorKapczinski, Flavio
dc.contributor.authorGallitano, Amelia L.
dc.contributor.authorKlamt, Fábio
dc.date.accessioned2018-03-14T17:28:12Z
dc.date.available2018-03-14T17:28:12Z
dc.date.issued2018-02-05
dc.identifier.citationEGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorder 2018, 12 Frontiers in Behavioral Neuroscienceen
dc.identifier.issn1662-5153
dc.identifier.doi10.3389/fnbeh.2018.00015
dc.identifier.urihttp://hdl.handle.net/10150/627052
dc.description.abstractBipolar 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.
dc.description.sponsorshipBrazilian 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]en
dc.language.isoenen
dc.publisherFRONTIERS MEDIA SAen
dc.relation.urlhttp://journal.frontiersin.org/article/10.3389/fnbeh.2018.00015/fullen
dc.rights© 2018 Pfaffenseller, Kapczinski, Gallitano and Klamt. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).en
dc.subjectimmediate early genesen
dc.subjectearly growth response gene 3 (EGR3)en
dc.subjectbrain-derived neurotrophic factor (BDNF)en
dc.subjectbipolar disorderen
dc.subjectneuroplasticityen
dc.subjectregulatory networken
dc.titleEGR3 Immediate Early Gene and the Brain-Derived Neurotrophic Factor in Bipolar Disorderen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Coll Med, Dept Basic Med Scien
dc.identifier.journalFrontiers in Behavioral Neuroscienceen
dc.description.noteOpen access journal.en
dc.description.collectioninformationThis 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.en
dc.eprint.versionFinal published versionen
refterms.dateFOA2018-09-13T22:40:40Z
html.description.abstractBipolar 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.


Files in this item

Thumbnail
Name:
fnbeh-12-00015.pdf
Size:
1.294Mb
Format:
PDF
Description:
Final Published Version

This item appears in the following Collection(s)

Show simple item record