Induction of the α1-antichymotrypsin gene in the brain associated with TGF-β1 deficiency or systemic administration of endotoxin

Hiroshi Saito, Leonard D. Shultz, Mala Sinha, John Papaconstantinou

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

We report that mRNA levels for α1-antichymotrypsin (ACT), a component of β-amyloid plaques in Alzheimer's disease, are significantly increased in the brains of two different mouse models that develop inflammation: (1) acute inflammation caused by intraperitoneal injection with lipopolysaccharide (LPS) and (2) chronic inflammation in knockout mice lacking the anti-inflammatory cytokine transforming growth factor β1 (TGF-β1). While brain mRNA levels for the inflammatory cytokines TNFα, IL-1β, and IL-6 were all elevated in the LPS-injected mice, only the mRNA for IL-1β increased significantly in TGF-β1-deficient mice. The transcription factor C/EBPβ was strongly activated in the brains of both models. These results support the hypothesis that, through induction of the ACT gene in the brain, inflammation plays an important role during the development of Alzheimer's disease and that IL-1β and C/EBPβ may be involved in this process.

Original languageEnglish (US)
Pages (from-to)270-275
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume263
Issue number2
DOIs
StatePublished - Sep 24 1999

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Transforming Growth Factors
Interleukin-1
Endotoxins
Brain
Genes
Inflammation
Messenger RNA
Lipopolysaccharides
Cytokines
Amyloid Plaques
Encephalitis
Intraperitoneal Injections
Knockout Mice
Interleukin-6
Alzheimer Disease
Anti-Inflammatory Agents
Transcription Factors
Amyloid

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Induction of the α1-antichymotrypsin gene in the brain associated with TGF-β1 deficiency or systemic administration of endotoxin. / Saito, Hiroshi; Shultz, Leonard D.; Sinha, Mala; Papaconstantinou, John.

In: Biochemical and Biophysical Research Communications, Vol. 263, No. 2, 24.09.1999, p. 270-275.

Research output: Contribution to journalArticle

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