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Fragmentation of phospholipid bilayers by myelin basic protein

M Roux1, F A Nezil, M Monck

  • 1Department of Physics, University of British Columbia, Vancouver, Canada.

Biochemistry
|January 11, 1994
PubMed

Insights

Human myelin basic protein (MBP) fragments lipid bilayers, similar to melittin. Negatively charged phosphatidylserine prevents this, but calcium ions abolish its effect, suggesting a role in demyelinating diseases.

Area of Science:

  • Biochemistry
  • Biophysics
  • Neuroscience

Background:

  • Myelin basic protein (MBP) is a key component of the myelin sheath.
  • Lipid bilayers form the structural basis of cell membranes.
  • Demyelinating diseases involve damage to the myelin sheath.

Purpose of the Study:

  • To investigate the effect of human myelin basic protein (MBP) on phosphatidylcholine bilayers.
  • To elucidate the mechanism of MBP-induced membrane disruption.
  • To explore the potential role of MBP in demyelinating diseases.

Main Methods:

  • Multilamellar phosphatidylcholine bilayers were used as a model system.
  • 31P nuclear magnetic resonance (NMR) spectroscopy monitored bilayer fragmentation.
  • Lipid composition, including phosphatidylserine and calcium ions, was varied.

Main Results:

  • MBP disrupted phosphatidylcholine bilayers into lipoprotein particles, similar to melittin.
  • Bilayer fragmentation was temperature-dependent.
  • Negatively charged phosphatidylserine inhibited fragmentation, an effect lost upon calcium ion binding.
  • MBP did not fragment bilayers mimicking myelin lipid composition.

Conclusions:

  • MBP can induce bilayer fragmentation in vitro.
  • Phosphatidylserine stabilizes membranes against MBP-induced disruption.
  • Calcium ions neutralize the stabilizing effect of phosphatidylserine.
  • MBP-induced membrane fragmentation may contribute to the pathogenesis of demyelinating diseases.

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