Midkine, a new neurotrophic factor, is present in glial cytoplasmic inclusions of multiple system atrophy brains

S Kato1, T Shinozawa, M Takikawa

  • 1Division of Neuropathology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.

Acta Neuropathologica
|October 25, 2000
PubMed

Insights

Midkine (MK) is present in glial cytoplasmic inclusions (GCIs) of multiple system atrophy (MSA) brains. This finding suggests a potential role for MK in a regenerative process within affected oligodendrocytes and neurons.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Glial cytoplasmic inclusions (GCIs) are a key histological feature of multiple system atrophy (MSA).
  • These inclusions, found in oligodendrocytes, comprise abnormal granule-coated fibrils.
  • The role of midkine (MK) within these GCIs is not well understood.

Purpose of the Study:

  • To investigate the significance of midkine (MK) presence in glial cytoplasmic inclusions (GCIs) in multiple system atrophy (MSA).

Main Methods:

  • Immunohistochemical analysis of MSA and control brains using an anti-MK antibody.
  • Electron and immunoelectron microscopy to visualize MK within GCIs.
  • Western blot analysis to confirm MK presence in MSA brains.

Main Results:

  • Most GCIs in MSA brains showed intense staining for MK.
  • GCIs were found to be composed of MK-positive granule-coated fibrils.
  • MK immunoreactivity was absent in oligodendrocytes, astrocytes, and neurons of normal control subjects.
  • Western blotting confirmed the presence of MK in MSA brains but not in normal brains.

Conclusions:

  • The presence of MK in GCIs suggests its essential role in the composition of these inclusions.
  • MK's association with fetal morphogenesis may indicate an endogenous repair mechanism in degenerated oligodendrocytes.
  • This potential repair mechanism might involve the oligodendrocyte-axon-neuron relationship in MSA.

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