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Effects of Alzheimer's peptide and alpha 1-antichymotrypsin on astrocyte gene expression

Baker, Crystal; Nielsen, Henrietta LU ; Minthon, Lennart LU ; Wright, H. T.; Chappell, Sally; Okyere, John; May, Sean; Morgan, Kevin; Kalsheker, Noor and Janciauskiene, Sabina LU (2007) In Neurobiology of Aging 28(1). p.51-61
Abstract
We employed gene array technology to investigate the effects of alpha 1-antichymotrypsin (ACT), soluble or fibrillar Alzheimer's peptide (A beta(1-42)) alone and the combination of ACT/A beta(1-42) on human astrocytes. Using a 1.2-fold change as significance threshold, 398 astrocyte genes showed altered expression in response to these treatments compared to controls. Of the 276 genes affected by the ACT/soluble A beta(1-42) combination, 195 (70.6%) were suppressed. The ACT/fibrillar A beta(1-42) combination affected expression of 64 genes of which 58 (90.5%) were up-regulated. The most prominent gene expression changes in response to the ACT/soluble A beta(1-42), were the down-regulation of at least 60 genes involved in transcription,... (More)
We employed gene array technology to investigate the effects of alpha 1-antichymotrypsin (ACT), soluble or fibrillar Alzheimer's peptide (A beta(1-42)) alone and the combination of ACT/A beta(1-42) on human astrocytes. Using a 1.2-fold change as significance threshold, 398 astrocyte genes showed altered expression in response to these treatments compared to controls. Of the 276 genes affected by the ACT/soluble A beta(1-42) combination, 195 (70.6%) were suppressed. The ACT/fibrillar A beta(1-42) combination affected expression of 64 genes of which 58 (90.5%) were up-regulated. The most prominent gene expression changes in response to the ACT/soluble A beta(1-42), were the down-regulation of at least 60 genes involved in transcription, signal transduction, apoptosis and neurogenesis. The ACT/fibril A beta(1-42) increased the expression of genes involved in transcription regulation and signal transduction. Surprisingly, gene expression of astrocytes exposed to soluble or fibrillar A beta(1-42) alone was largely unaffected. Thus, the molecular forms generated by the combination of ACT/A beta(1-42) alter expression of astrocyte genes more profoundly in breadth and magnitude than soluble or fibrillar A beta(1-42) alone, suggesting that pathogenic effects of A beta(1-42) may occur as a consequence of its association with other proteins. (c) 2005 Elsevier Inc. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
inflammation, gene expression, Alzheimer's disease, alpha 1-antichymotrypsin, Alzheimer's peptide (A beta 42), astrocytes
in
Neurobiology of Aging
volume
28
issue
1
pages
51 - 61
publisher
Elsevier
external identifiers
  • wos:000242740100007
  • scopus:33751226575
ISSN
1558-1497
DOI
10.1016/j.neurobiolaging.2005.10.017
language
English
LU publication?
yes
id
286ed293-bb50-4601-970d-11f5c0c099fb (old id 682430)
date added to LUP
2007-12-07 13:21:10
date last changed
2017-11-19 03:35:36
@article{286ed293-bb50-4601-970d-11f5c0c099fb,
  abstract     = {We employed gene array technology to investigate the effects of alpha 1-antichymotrypsin (ACT), soluble or fibrillar Alzheimer's peptide (A beta(1-42)) alone and the combination of ACT/A beta(1-42) on human astrocytes. Using a 1.2-fold change as significance threshold, 398 astrocyte genes showed altered expression in response to these treatments compared to controls. Of the 276 genes affected by the ACT/soluble A beta(1-42) combination, 195 (70.6%) were suppressed. The ACT/fibrillar A beta(1-42) combination affected expression of 64 genes of which 58 (90.5%) were up-regulated. The most prominent gene expression changes in response to the ACT/soluble A beta(1-42), were the down-regulation of at least 60 genes involved in transcription, signal transduction, apoptosis and neurogenesis. The ACT/fibril A beta(1-42) increased the expression of genes involved in transcription regulation and signal transduction. Surprisingly, gene expression of astrocytes exposed to soluble or fibrillar A beta(1-42) alone was largely unaffected. Thus, the molecular forms generated by the combination of ACT/A beta(1-42) alter expression of astrocyte genes more profoundly in breadth and magnitude than soluble or fibrillar A beta(1-42) alone, suggesting that pathogenic effects of A beta(1-42) may occur as a consequence of its association with other proteins. (c) 2005 Elsevier Inc. All rights reserved.},
  author       = {Baker, Crystal and Nielsen, Henrietta and Minthon, Lennart and Wright, H. T. and Chappell, Sally and Okyere, John and May, Sean and Morgan, Kevin and Kalsheker, Noor and Janciauskiene, Sabina},
  issn         = {1558-1497},
  keyword      = {inflammation,gene expression,Alzheimer's disease,alpha 1-antichymotrypsin,Alzheimer's peptide (A beta 42),astrocytes},
  language     = {eng},
  number       = {1},
  pages        = {51--61},
  publisher    = {Elsevier},
  series       = {Neurobiology of Aging},
  title        = {Effects of Alzheimer's peptide and alpha 1-antichymotrypsin on astrocyte gene expression},
  url          = {http://dx.doi.org/10.1016/j.neurobiolaging.2005.10.017},
  volume       = {28},
  year         = {2007},
}