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Hyperfibrinogenemia-mediated astrocyte activation.

Vincent D Clark1, Ailey Layson1, Mariam Charkviani1

  • 1Department of Physiology, University of Louisville, School of Medicine, Louisville, KY, USA.

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|August 29, 2018
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Summary

Fibrinogen (Fg) activates brain astrocytes by increasing intercellular adhesion molecule 1 (ICAM-1) and tyrosine receptor kinase B (TrkB) signaling. This astrocyte activation may contribute to memory loss in neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Fibrinogen (Fg) plaques correlate with memory loss in neurodegenerative diseases like Alzheimer's.
  • The precise role of Fg in the neurovascular unit remains unclear.
  • Fg's high molecular weight suggests localized interactions, potentially with astrocytes.

Purpose of the Study:

  • To investigate the mechanism by which Fg interacts with astrocytes.
  • To determine if Fg binding to astrocytes leads to astrocyte activation.
  • To explore the role of intercellular adhesion molecule 1 (ICAM-1) in Fg-induced astrocyte activation.

Main Methods:

  • Primary mouse cortical astrocytes were cultured and treated with Fg.
  • Intercellular adhesion molecule 1 (ICAM-1) function was blocked using an antibody.
  • Astrocyte activation markers, including ICAM-1 and tyrosine receptor kinase B (TrkB) expression and TrkB phosphorylation (pTrkB), were measured.

Main Results:

  • Fg dose-dependently induced astrocyte activation, characterized by morphological changes and process retraction.
  • Fg significantly increased the expression of ICAM-1 and TrkB, along with elevated pTrkB levels.
  • Blocking ICAM-1 function partially reversed the Fg-induced astrocyte activation.

Conclusions:

  • Fg interacts with astrocytes, triggering overexpression of ICAM-1 and TrkB, and promoting TrkB phosphorylation.
  • This Fg-induced astrocyte activation, involving TrkB signaling, may be a key mechanism underlying memory deficits in neurodegenerative conditions.
  • Fg's interaction with astrocytes represents a potential therapeutic target for mitigating cognitive decline associated with neuroinflammation.