Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

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)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and
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
  • pmid:16364502
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
2016-04-01 12:17:44
date last changed
2022-01-27 01:39:35
@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}},
  keywords     = {{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}},
  doi          = {{10.1016/j.neurobiolaging.2005.10.017}},
  volume       = {{28}},
  year         = {{2007}},
}