Induction of protein kinase C substrates, Myristoylated alanine-rich C kinase substrate (MARCKS) and MARCKS-related protein (MRP), by amyloid β-protein in mouse BV-2 microglial cells

Anne Murphy, Janet R. Sunohara, Meenakshi Sundaram, Neale D. Ridgway, Christopher R. McMaster, Harold W. Cook, David M. Byers

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

10 Citas (Scopus)

Resumen

Microglial activation by amyloid β-protein in senile plaques contributes to neurodegeneration in Alzheimer disease. In BV-2 microglial cells, amyloid β-protein 1-40 (Aβ 1-40) elicited a dose-dependent increase (3-4 fold) of Myristoylated alanine-rich C kinase substrate (MARCKS) and MARCKS-related protein (MRP), two protein kinase C substrates implicated in membrane-cytoskeletal alterations underlying microglial adhesion, migration, secretion, and phagocytosis. Neither MARCKS nor MRP was induced by the amyloid fragment Aβ 25-35, although both Aβ 1-40 and Aβ 25-35 caused extensive aggregation of BV-2 cells. Interferon-γ synergistically enhanced the induction by Aβ 1-40 of inducible nitric oxide synthase, but not MARCKS or MRP. Our results suggest that MARCKS and MRP may play important roles in microglia activated by amyloid peptides.

Idioma originalEnglish
Páginas (desde-hasta)9-12
Número de páginas4
PublicaciónNeuroscience Letters
Volumen347
N.º1
DOI
EstadoPublished - ago. 14 2003

ASJC Scopus Subject Areas

  • General Neuroscience

PubMed: MeSH publication types

  • Journal Article

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