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Rapid Generation of Amyloid from Native Proteins In vitro
05:48

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

Beta amyloid peptide (Abeta42) is internalized via the G-protein-coupled receptor FPRL1 and forms fibrillar

H Yazawa1, Z X Yu, Takeda

  • 1Laboratory of Molecular Immunoregulation, SAIC Frederick, Center for Cancer Research, National Cancer Institute at Frederick, Maryland 21702, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|November 2, 2001
PubMed

Insights

The G-protein-coupled receptor FPRL1 facilitates the uptake of beta amyloid (Abeta42) into cells. Persistent Abeta42 exposure leads to fibril formation in macrophages via FPRL1.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Beta amyloid (Abeta42) is implicated in Alzheimer's disease (AD) neurotoxicity and mononuclear phagocyte activation.
  • FPRL1, a G-protein-coupled receptor, mediates Abeta42's effects on monocytes and microglia, suggesting its role in AD neuroinflammation.

Purpose of the Study:

  • To investigate the role of FPRL1 in the cellular uptake and fibril formation of Abeta42.
  • To elucidate the mechanism of Abeta42 internalization and subsequent aggregation in cells expressing FPRL1.

Main Methods:

  • Fluorescence confocal microscopy was employed to visualize Abeta42-FPRL1 interactions.
  • Macrophages and genetically engineered HEK293 cells expressing FPRL1 were used to study Abeta42 uptake and fibril formation.

Main Results:

  • Abeta42 rapidly associated with and was internalized into FPRL1-expressing cells (macrophages, HEK293) within 30 minutes.
  • FPRL1 recycled to the cell surface upon Abeta42 removal, while internalized Abeta42 was degraded.
  • Prolonged Abeta42 exposure (24h) led to Abeta42/FPRL1 complex retention and Congo red-positive fibril formation specifically in macrophages, not HEK293 cells.

Conclusions:

  • FPRL1 mediates Abeta42 internalization and contributes to fibril formation in macrophages.
  • The cellular context (macrophage vs. HEK293) influences Abeta42 fibril formation following FPRL1-mediated uptake.

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