Gene expression profiling in postmortem prefrontal cortex of major depressive disorder

Investigations of the molecular mechanisms underlying major depressive disorder (MDD) have been hampered by the complexity of brain tissue and sensitivity of gene expression profiling approaches. To address these issues, we used discrete microdissections of postmortem dorsolateral prefrontal cortex...

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Vydané v:The Journal of neuroscience Ročník 27; číslo 48; s. 13329
Hlavní autori: Kang, Hyo Jung, Adams, David H, Simen, Arthur, Simen, Birgitte B, Rajkowska, Grazyna, Stockmeier, Craig A, Overholser, James C, Meltzer, Herbert Y, Jurjus, George J, Konick, Lisa C, Newton, Samuel S, Duman, Ronald S
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 28.11.2007
Predmet:
Adult
Aged
Case-Control Studies
Cell Cycle - genetics
Cell Death
Cell Differentiation - genetics
Depressive Disorder, Major - pathology
Female
Forkhead Transcription Factors - metabolism
Gene Expression - physiology
Gene Expression Profiling - methods
Humans
In Situ Hybridization - methods
Male
Middle Aged
Multivariate Analysis
Oligonucleotide Array Sequence Analysis - methods
Postmortem Changes
Prefrontal Cortex - metabolism
Prefrontal Cortex - physiopathology
Signal Transduction - genetics
Transcription Factors
ISSN:1529-2401, 1529-2401
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Popis
Shrnutí:Investigations of the molecular mechanisms underlying major depressive disorder (MDD) have been hampered by the complexity of brain tissue and sensitivity of gene expression profiling approaches. To address these issues, we used discrete microdissections of postmortem dorsolateral prefrontal cortex (DLPFC) (area 9) and an oligonucleotide (60mer) microarray hybridization procedure that increases sensitivity without RNA amplification. Mixed-effects statistical methods were used to rigorously control for medication usage in the subset of medicated depressed subjects. These analyses yielded a rich profile of dysregulated genes. Two of the most highly dysregulated genes of interest were stresscopin, a neuropeptide involved in stress responses, and Forkhead box D3 (FOXD3), a transcription factor. Secondary cell-based analysis demonstrated that stresscopin and FoxD3 are increased in neurons of DLPFC gray matter of MDD subjects. These findings identify abnormal gene expression in a discrete region of MDD subjects and contribute to further elucidation of the molecular alterations of this complex mood disorder.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1529-2401
1529-2401
DOI:10.1523/jneurosci.4083-07.2007