β‐Amyloid1–40 Increases Expression of β‐Amyloid Precursor Protein in Neuronal Hybrid Cells

Weidong Le, Wen Jie Xie, Okot Nyormoi, Bao Kuang Ho, R. Glenn Smith, Stanley H. Appel

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Studies of cell injury and death in Alzheimer's disease have suggested a prominent role for β-amyloid peptide (β-AP), a 40-43-amino-acid peptide derived from a larger membrane glycoprotein, β-amyloid precursor protein (β-APP). Previous experiments have demonstrated that β-AP induces cytotoxicity in a neuronal hybrid cell line (MES 23.5) in vitro. Here, we demonstrate that β-APP mRNA content is increased 3.5-fold in 24 h after treatment with β-AP1-40. Accompanying β-AP1-40-induced cell injury, levels of cell-associated β-APP and a C-terminal intermediate fragment are increased up to 15-fold, and levels of secreted forms of β-APP and 12- and 4-kDa fragments are also increased. Application of β-APP antisense oligodeoxynucleotide reduces both cytotoxicity and β-APP expression. 6-Hydroxydopamine application or glucose deprivation causes extensive cell damage, but they do not increase β-APP expression. These results suggest a selective positive feedback mechanism whereby β-AP may induce cytotoxicity and increase levels of potentially neurotrophic as well as amyloidogenic fragments of β-APP with the net consequence of further neuronal damage.

Original languageEnglish (US)
Pages (from-to)2373-2376
Number of pages4
JournalJournal of Neurochemistry
Volume65
Issue number5
DOIs
StatePublished - Nov 1995

Keywords

  • β-Amyloid peptide
  • β-Amyloid precursor protein-Neuronal hybrid cell line
  • Alzheimer's disease
  • Cytotoxicity

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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