Human amyloid-β causes changes in the levels of endothelial protein kinase C and its α isoform in vitro

M. Pákáski, Lajos Balaspiri, Frederic Checler, P. Kása

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Amyloid-β (Aβ) deposits and neurofibrillary pathology are characteristic features of Alzheimer's disease (AD). The association of Aβ with cerebral vessels is an intriguing feature of AD. While there is considerable evidence of altered activities of the major isoforms of protein kinase C (PKC) in the vasculature and neurons of AD brains, little is known about the relationship between the Aβ toxicity and the altered PKC levels in cerebral endothelial cells. In this study, cultured brain endothelial cells exposed to Aβ1-40 revealed a translocation of PKC from the membrane fraction to the cytosol. The content of the isoform PKCα, involved in the regulation of amyloid precursor protein (APP) secretion, was decreased in the membrane-bound fraction of rat endothelial cells and increased in the cytosol after Aβ1-40 treatment. These data suggest that the accumulation of Aβ peptide in the cerebral vasculature may play a significant role in the down-regulation of PKC seen in the AD cerebral vasculature.

Original languageEnglish
Pages (from-to)409-414
Number of pages6
JournalNeurochemistry International
Volume41
Issue number6
DOIs
Publication statusPublished - Dec 2002

Fingerprint

Amyloid
Protein Kinase C
Protein Isoforms
Alzheimer Disease
Endothelial Cells
Cytosol
Membranes
Amyloid beta-Protein Precursor
Amyloid Plaques
Brain
Down-Regulation
In Vitro Techniques
Pathology
Neurons
Peptides

Keywords

  • Alzheimer's disease
  • Amyloid
  • Endothelial culture
  • Immunoblotting
  • Immunohistochemistry
  • PKC

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

Human amyloid-β causes changes in the levels of endothelial protein kinase C and its α isoform in vitro. / Pákáski, M.; Balaspiri, Lajos; Checler, Frederic; Kása, P.

In: Neurochemistry International, Vol. 41, No. 6, 12.2002, p. 409-414.

Research output: Contribution to journalArticle

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