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Effect of a carboxy-terminal fragment of the Alzheimer's amyloid precursor protein on expression of proinflammatory cytokines in rat glial cells

Title
Effect of a carboxy-terminal fragment of the Alzheimer's amyloid precursor protein on expression of proinflammatory cytokines in rat glial cells
Authors
Chong Y.
Ewha Authors
정영해
SCOPUS Author ID
정영해scopus
Issue Date
1997
Journal Title
Life Sciences
ISSN
0024-3205JCR Link
Citation
vol. 61, no. 23, pp. 2323 - 2333
Indexed
SCI; SCIE; SCOPUS scopus
Abstract
To explore factors involved in the induction of cytokines that may contribute to the pathogenesis of Alzheimer's disease (AD), the effect of a carboxy terminal 105 amino acid fragment (CT105) of the amyloid precursor protein (APP) on the gene expression of proinflammatory cytokines, IL-1β and IL-6 was determined in cultured rat cortical glial cells in comparison to amyloid beta protein (Aβ). Cells were incubated with 1 μM of insoluble CT105 aggregates or aged Aβ1-40 peptide deposits which were mainly composed of stable monomeric and dimeric forms as assessed on Western blots. The levels of mRNAs were analyzed by reverse transcription polymerase chain reaction (RT-PCR). Highest levels of both IL-1β and IL-6 transcripts were detected in the culture exposed to CT105 aggregates for 4 days. CT105 aggregates markedly increased IL-1β mRNA level by 3.5 fold of the control level and this effect was more potent than that produced by aged Aβ1-40 peptides. Furthermore, CT105 strongly induced accumulation of IL-6 mRNA level by 2 fold of the value potentiated by Aβ1-40. Such induction was not observed with Aβ 12-28 treatment. On the other hand, CT105 did not significantly alter either APP or glial fibrillary acidic protein (GFAP) mRNA levels. These results together imply that CT peptide besides its cytotoxic potency may act as a potent immunological component, strongly inducing both IL-1β and IL-6 mRNA levels in the cultured glial cells. This CT peptide associated exacerbation of cytokine expression may be in part responsible for chronic inflammation linked to slowly progressive neurodegeneration characteristic to AD.
DOI
10.1016/S0024-3205(97)00936-3
Appears in Collections:
의과대학 > 의학과 > Journal papers
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