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Apolipoprotein E inhibits the depolymerization of beta 2-microglobulin-related amyloid fibrils at a neutral pH

I Yamaguchi1, K Hasegawa, N Takahashi

  • 1Department of Pathology, Fukui Medical University, Fukui 910-1193, Japan.

Biochemistry
|July 18, 2001
PubMed

Insights

Beta 2-microglobulin (beta 2-m) amyloid fibrils depolymerize at neutral to basic pH. Apolipoprotein E stabilizes these fibrils, potentially enhancing amyloid deposition in vivo.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Medical Science

Background:

  • Beta 2-microglobulin (beta 2-m) amyloidosis is a serious complication for hemodialysis patients.
  • Beta 2-microglobulin (beta 2-m) is a key structural component of amyloid fibrils.

Purpose of the Study:

  • To investigate the depolymerization of beta 2-microglobulin amyloid fibrils.
  • To determine the effect of apolipoprotein E (apoE) on beta 2-m amyloid fibril stability.

Main Methods:

  • Fluorescence spectroscopy (Thioflavin T) and electron microscopy were used to study A beta 2M amyloid fibrils.
  • Circular dichroism analyzed conformational changes during depolymerization.
  • Apolipoprotein E's interaction with A beta 2M amyloid fibrils was assessed.

Main Results:

  • A beta 2M amyloid fibrils depolymerize into monomeric beta 2-m at neutral to basic pH.
  • Apolipoprotein E formed a stable complex with A beta 2M amyloid fibrils.
  • Apolipoprotein E inhibited fibril depolymerization in a dose-dependent manner.

Conclusions:

  • A beta 2-microglobulin amyloid fibrils are unstable at neutral to basic pH.
  • Apolipoprotein E stabilizes beta 2-m amyloid fibrils by binding to them.
  • Apolipoprotein E may enhance in vivo amyloid deposition by stabilizing beta 2-m fibrils.

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