Effects of Alzheimer's peptide and alpha 1-antichymotrypsin on astrocyte gene expression
(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:
https://lup.lub.lu.se/record/682430
- author
- 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
- organization
- publishing date
- 2007
- 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}},
}