β-Amyloid-specific upregulation of stearoyl coenzyme A desaturase-1 in macrophages

• Published in: Biochemical and biophysical research communications Vol. 303; no. 1; pp. 302 - 305
• Main Authors: Uryu, Shigeko, Tokuhiro, Shinya, Oda, Tomiichiro
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 28.03.2003
• Subjects: Alzheimer Disease - metabolism; Alzheimer’s disease; Amyloid beta-Peptides - metabolism; Animals; Humans; Inflammation; Interferon-gamma - metabolism; Macrophages - enzymology; Macrophages - metabolism; Macrophages, Peritoneal - metabolism; Mice; Microarray; Microglia; Oligonucleotide Array Sequence Analysis; Pyrimidines - pharmacology; Reverse Transcriptase Polymerase Chain Reaction; RNA - metabolism; RNA, Messenger - metabolism; Stearoyl coenzyme A desaturase; Stearoyl-CoA Desaturase - chemistry; Stearoyl-CoA Desaturase - genetics; Time Factors; Up-Regulation; β-Amyloid; β-Amyloid; Inflammation; Stearoyl coenzyme A desaturase; Alzheimer’s disease; Microarray; Microglia
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/S0006-291X(03)00334-6

β-Amyloid peptide (Aβ), a major component of senile plaques, the formation of which is characteristic of Alzheimer’s disease (AD), is believed to induce inflammation of the brain mediated by microglia, leading to neuronal cell loss. In this study, we performed an oligonucleotide microarray analysis to investigate the molecular events underlying the Aβ-induced activation of macrophages and its specific suppression by the Aβ-specific-macrophage-activation inhibitor, RS-1178. Of the approximately 36,000 genes and expressed sequence tags analyzed, eight genes were specifically and significantly upregulated by a treatment with interferon γ (IFNγ) and Aβ compared to a treatment with IFNγ alone ( p<0.002). We found that the gene for a well-characterized lipogenetic enzyme, stearoyl coenzyme A desaturase-1 (SCD-1), was specifically upregulated by Aβ treatment and was suppressed to basal levels by RS-1178. Although the underlying mechanisms remain unknown, our results suggest the presence of a link between AD and SCD-1.