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Nanomolar aluminum induces pro-inflammatory and pro-apoptotic gene expression in human brain cells in primary culture.

Abstract：

:Aluminum, the most abundant neurotoxic metal in our biosphere, has been implicated in the etiology of several neurodegenerative disorders including Alzheimer's disease (AD). To further understand aluminum's influence on gene expression, we examined total messenger RNA levels in untransformed human neural cells exposed to 100 nanomolar aluminum sulfate using high density DNA microarrays that interrogate the expression of every human gene. Preliminary data indicate that of the most altered gene expression levels, 17/24 (70.8%) of aluminum-affected genes, and 7/8 (87.5%) of aluminum-induced genes exhibit expression patterns similar to those observed in AD. The seven genes found to be significantly up-regulated by aluminum encode pro-inflammatory or pro-apoptotic signaling elements, including NF-kappaB subunits, interleukin-1beta precursor, cytosolic phospholipase A2, cyclooxygenase-2, beta-amyloid precursor protein and DAXX, a regulatory protein known to induce apoptosis and repress transcription. The promoters of genes up-regulated by aluminum are enriched in binding sites for the stress-inducible transcription factors HIF-1 and NF-kappaB, suggesting a role for aluminum, HIF-1 and NF-kappaB in driving atypical, pro-inflammatory and pro-apoptotic gene expression. The effect of aluminum on specific stress-related gene expression patterns in human brain cells clearly warrant further investigation.

journal_name

J Inorg Biochem

journal_title

Journal of inorganic biochemistry

authors

Lukiw WJ,Percy ME,Kruck TP

doi

10.1016/j.jinorgbio.2005.04.021

subject

Has Abstract

pub_date

2005-09-01 00:00:00

pages

1895-8

issue

9

eissn

0162-0134

issn

1873-3344

pii

S0162-0134(05)00118-2

journal_volume

99

pub_type

杂志文章

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