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Related Experiment Videos

Sulfation of rat apolipoprotein E.

P J Gebicke-Haerter1, E M Shooter

  • 1Department of Neurobiology, Stanford University School of Medicine, California.

Journal of Neurochemistry
|September 1, 1989
PubMed
Summary

Nerve injury increases apolipoprotein E (apo-E) synthesis in rats. This protein

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Area of Science:

  • Neuroscience
  • Biochemistry

Background:

  • Apolipoprotein E (apo-E) is a 37-kDa protein implicated in nerve repair.
  • Previous studies showed increased apo-E synthesis after sciatic nerve injury.

Purpose of the Study:

  • To investigate apo-E synthesis and modification in the rat optic nerve after injury.
  • To characterize the sialylation and sulfation of apo-E in different nervous tissues and cell cultures.

Main Methods:

  • Time-course studies of apo-E synthesis in injured rat optic nerves.
  • Two-dimensional electrophoresis and neuraminidase treatment to analyze apo-E.
  • 35SO4 incorporation studies in cultured optic nerve explants, glial cells, and macrophages.

Main Results:

  • Optic nerve injury induced a delayed but sustained increase in apo-E synthesis.
  • Apo-E "trailing" in electrophoresis is due to sialylation, differing between CNS and peripheral nervous tissue.
  • CNS glial cells and macrophages sulfated apo-E, unlike Schwann cells.

Conclusions:

  • Macrophages are a likely source of apo-E in injured nerves and glial cultures.
  • Sciatic nerve cells may secrete sulfatases, affecting apo-E sialic acid residues.
  • Differences in apo-E modification exist between central and peripheral nervous systems during regeneration.

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