S100β increases levels of β-amyloid precursor protein and its encoding mRNA in rat neuronal cultures

Yuekui Li, Jianzhong Wang, Jin G. Sheng, Ling Liu, Steven W. Barger, Richard A. Jones, Linda J. Van Eldik, Robert E. Mrak, W. Sue T. Griffin

Research output: Contribution to journalArticlepeer-review

110 Scopus citations

Abstract

S100β has been implicated in the formation of dystrophic neurites, overexpressing β-amyloid precursor protein (βAPP), in the β-amyloid plaques of Alzheimer's disease. We assessed the effects of S100β on cell viability of, neurite outgrowth from, and βAPP expression by neurons in primary cultures from fetal rat cortex. S100β (1-10 ng/ml) enhanced neuronal viability (as assessed by increased mitrochondrial activity and decreased lactic acid dehydrogenase release) and promoted neurite outgrowth. Higher levels of S100β (100 ng/ml, but not 1 μg/ml) produced qualitatively similar, but less marked, effects. S100β also induced increased neuronal expression of the microtubule-associated protein MAP2, an effect that is consistent with trophic effects of S100β on neurite outgrowth. S100β (10 and 100 ng/ml) induced graded increases in neuronal expression of βAPP and of βAPP mRNA. These results support our previous suggestion that excessive expression of S100β by activated, plaque-associated astrocytes in Alzheimer's disease contributes to the appearance of dystrophic neurites overexpressing βAPP in diffuse amyloid deposits, and thus to the conversion of these deposits into the diagnostic neuritic β-amyloid plaques.

Original languageEnglish
Pages (from-to)1421-1428
Number of pages8
JournalJournal of Neurochemistry
Volume71
Issue number4
DOIs
StatePublished - Oct 1998

Keywords

  • Alzheimer's disease
  • In situ hybridization
  • Northern hybridization
  • S100β
  • Western immunoblot
  • β-Amyloid precursor protein

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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