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Triggering Reactive Gliosis In Vivo by a Forebrain Stab Injury
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Abnormal mitosis in reactive astrocytes.

Alexander Sosunov1, Xiaoping Wu1, Robert McGovern2

  • 1Department of Neurosurgery, Columbia University, 630 W. 168th St, P&S 15-405, New York, NY, 10032, USA.

Acta Neuropathologica Communications
|April 16, 2020
PubMed
Summary

Reactive astrocytes exhibit abnormal mitosis without cell division, leading to polyploidy and micronuclei formation. This pathology arises from spindle defects and cellular constraints, impacting astrocyte cell cycle progression.

Keywords:
AstrocytesCreutzfeldt-Peters cellsMitosisMitotic spindlesPolyploidy

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Abnormal mitosis in astrocytes, termed
  • Alzheimer I type astrocytes
  • or
  • Creutzfeldt-Peters cells
  • , has been documented for a century.
  • The underlying mechanisms and origins of this astrocyte pathology remain poorly understood.

Purpose of the Study:

  • To investigate the mechanisms of abnormal mitosis in reactive astrocytes.
  • To elucidate the origins of micronuclei formation and polyploidy in astrocytes following brain insults.

Main Methods:

  • Induction of experimental brain insults in a rat model.
  • Microscopic analysis of astrocyte mitosis and cell cycle progression.
  • Assessment of mitotic spindle formation and chromosome dynamics.

Main Results:

  • Abnormal mitoses, specifically those lacking cytokinesis, are characteristic of reactive astrocytes.
  • Pathology stems from defects in mitotic spindle formation and chromosome alignment, potentially due to cellular enlargement and protein accumulation.
  • Astrocyte cell cycle arrest is often circumvented by micronuclei formation, resulting in polyploid cells.
  • These polyploid astrocytes demonstrate long-term survival and re-entry into subsequent cell cycles.

Conclusions:

  • Abnormal mitosis and polyploidy in reactive astrocytes are driven by impaired cell division processes.
  • Micronuclei formation represents an escape mechanism from mitotic arrest, leading to viable polyploid astrocytes.
  • Understanding these mechanisms is crucial for comprehending astrocyte responses to brain injury and potential roles in neurological diseases.