Abstract:
:The identification of key genes in transcriptomic data constitutes a huge challenge. Our review of microarray reports revealed 88 genes whose transcription is consistently regulated by glucocorticoids (GCs), such as cortisol, corticosterone and dexamethasone, in the brain. Replicable transcriptomic data were combined with biochemical and physiological data to create an integrated view of the effects induced by GCs. The most frequently reported genes were Errfi1 and Ddit4. Their up-regulation was associated with the altered transcription of genes regulating growth factor and mTORC1 signaling (Gab1, Tsc22d3, Dusp1, Ndrg2, Ppp5c and Sesn1) and progression of the cell cycle (Ccnd1, Cdkn1a and Cables1). The GC-induced reprogramming of cell function involves changes in the mRNA level of genes responsible for the regulation of transcription (Klf9, Bcl6, Klf15, Tle3, Cxxc5, Litaf, Tle4, Jun, Sox4, Sox2, Sox9, Irf1, Sall2, Nfkbia and Id1) and the selective degradation of mRNA (Tob2). Other genes are involved in the regulation of metabolism (Gpd1, Aldoc and Pdk4), actin cytoskeleton (Myh2, Nedd9, Mical2, Rhou, Arl4d, Osbpl3, Arhgef3, Sdc4, Rdx, Wipf3, Chst1 and Hepacam), autophagy (Eva1a and Plekhf1), vesicular transport (Rhob, Ehd3, Vps37b and Scamp2), gap junctions (Gjb6), immune response (Tiparp, Mertk, Lyve1 and Il6r), signaling mediated by thyroid hormones (Thra and Sult1a1), calcium (Calm2), adrenaline/noradrenaline (Adcy9 and Adra1d), neuropeptide Y (Npy1r) and histamine (Hdc). GCs also affected genes involved in the synthesis of polyamines (Azin1) and taurine (Cdo1). The actions of GCs are restrained by feedback mechanisms depending on the transcription of Sgk1, Fkbp5 and Nr3c1. A side effect induced by GCs is increased production of reactive oxygen species. Available data show that the brain's response to GCs is part of an emergency mode characterized by inactivation of non-core activities, restrained inflammation, restriction of investments (growth), improved efficiency of energy production and the removal of unnecessary or malfunctioning cellular components to conserve energy and maintain nutrient supply during the stress response.
journal_name
Prog Neuropsychopharmacol Biol Psychiatryauthors
Juszczak GR,Stankiewicz AMdoi
10.1016/j.pnpbp.2017.11.020subject
Has Abstractpub_date
2018-03-02 00:00:00pages
136-168eissn
0278-5846issn
1878-4216pii
S0278-5846(17)30463-3journal_volume
82pub_type
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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pub_type: 杂志文章,多中心研究
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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更新日期:2005-02-01 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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更新日期:2014-10-03 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
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更新日期:2012-10-01 00:00:00
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journal_title:Progress in neuro-psychopharmacology & biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.pnpbp.2004.08.011
更新日期:2005-01-01 00:00:00