Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis

Down syndrome (trisomy 21) neurons display an increased rate of apoptosis in vitro. The genes on chromosome 21 that mediate this increased cell death remain to be elucidated. Here we show that the chromosome 21 transcription factor Ets2, a gene that is overexpressed in Down syndrome, is expressed in...

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Main Authors: E.J Wolvetang, O.M Bradfield, T Hatzistavrou, P.J Crack, J Busciglio, I Kola, P.J Hertzog
Format: Article
Language:English
Published: Elsevier 2003-12-01
Series:Neurobiology of Disease
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996103001074
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author E.J Wolvetang
O.M Bradfield
T Hatzistavrou
P.J Crack
J Busciglio
I Kola
P.J Hertzog
author_facet E.J Wolvetang
O.M Bradfield
T Hatzistavrou
P.J Crack
J Busciglio
I Kola
P.J Hertzog
author_sort E.J Wolvetang
collection DOAJ
description Down syndrome (trisomy 21) neurons display an increased rate of apoptosis in vitro. The genes on chromosome 21 that mediate this increased cell death remain to be elucidated. Here we show that the chromosome 21 transcription factor Ets2, a gene that is overexpressed in Down syndrome, is expressed in neurons, and that moderate overexpression of Ets2 leads to increased apoptosis of primary neuronal cultures from Ets2 tg mice that involves activation of caspase-3. Our data therefore suggest that overexpression of ETS2 may contribute to the increased rate of apoptosis of neurons in Down syndrome.
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spelling doaj.art-34e1ff2b1c2c42ea8e9748eda01ac0322022-12-21T18:36:25ZengElsevierNeurobiology of Disease1095-953X2003-12-01143349356Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosisE.J Wolvetang0O.M Bradfield1T Hatzistavrou2P.J Crack3J Busciglio4I Kola5P.J Hertzog6Centre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USACentre for Functional Genomics and Human Disease, Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, Clayton 3168, Australia; Department of Neuroscience, MC-3401, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USADown syndrome (trisomy 21) neurons display an increased rate of apoptosis in vitro. The genes on chromosome 21 that mediate this increased cell death remain to be elucidated. Here we show that the chromosome 21 transcription factor Ets2, a gene that is overexpressed in Down syndrome, is expressed in neurons, and that moderate overexpression of Ets2 leads to increased apoptosis of primary neuronal cultures from Ets2 tg mice that involves activation of caspase-3. Our data therefore suggest that overexpression of ETS2 may contribute to the increased rate of apoptosis of neurons in Down syndrome.http://www.sciencedirect.com/science/article/pii/S0969996103001074Ets transcription factorApoptosisDown syndromeβ-APPAlzheimer's diseaseEts2
spellingShingle E.J Wolvetang
O.M Bradfield
T Hatzistavrou
P.J Crack
J Busciglio
I Kola
P.J Hertzog
Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
Neurobiology of Disease
Ets transcription factor
Apoptosis
Down syndrome
β-APP
Alzheimer's disease
Ets2
title Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
title_full Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
title_fullStr Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
title_full_unstemmed Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
title_short Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis
title_sort overexpression of the chromosome 21 transcription factor ets2 induces neuronal apoptosis
topic Ets transcription factor
Apoptosis
Down syndrome
β-APP
Alzheimer's disease
Ets2
url http://www.sciencedirect.com/science/article/pii/S0969996103001074
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