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Related Experiment Video

Updated: Feb 19, 2026

Preparation of Rat Oligodendrocyte Progenitor Cultures and Quantification of Oligodendrogenesis Using Dual-infrared Fluorescence Scanning
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Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular

Mark A Petersen1, Jae Kyu Ryu2, Kae-Jiun Chang3

  • 1Gladstone Institutes, San Francisco, CA, USA; Department of Pediatrics, University of California, San Francisco, CA, USA.

Neuron
|November 7, 2017
PubMed
Summary

Fibrinogen, a blood protein, blocks brain repair by activating BMP signaling in oligodendrocyte progenitor cells (OPCs). Reducing fibrinogen enhances remyelination, offering a potential therapeutic strategy for neurological diseases.

Keywords:
NG2 cellsancrodcell fatefibrinmyelinneonatal brain injuryneuroinflammationregenerationstem/progenitor cellsvasculature

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Blood-brain barrier (BBB) disruption introduces blood proteins into the central nervous system (CNS).
  • The role of blood-derived molecules as inhibitors of central nervous system (CNS) remyelination remains unclear.

Purpose of the Study:

  • To investigate whether fibrinogen, a blood-derived molecule, inhibits remyelination.
  • To elucidate the molecular mechanisms by which fibrinogen affects oligodendrocyte progenitor cells (OPCs) and remyelination.

Main Methods:

  • In vitro studies using OPCs treated with fibrinogen.
  • Inhibition of bone morphogenetic protein (BMP) signaling pathway using DMH1 or ACVR1 knockout.
  • In vivo studies involving therapeutic depletion of fibrinogen.
  • Analysis of fibrinogen and BMP target Id2 in multiple sclerosis (MS) lesions.

Main Results:

  • Fibrinogen activates the BMP signaling pathway in OPCs, suppressing their differentiation into myelinating oligodendrocytes (OLs).
  • Fibrinogen promotes an astrocytic fate in OPCs in vitro.
  • Inhibition of BMP signaling or ACVR1 rescues fibrinogen-induced effects.
  • Fibrinogen and Id2 levels are elevated in demyelinated MS lesions.
  • Therapeutic fibrinogen depletion enhances remyelination in vivo.

Conclusions:

  • Fibrinogen acts as an extrinsic inhibitor of CNS remyelination by activating BMP signaling in OPCs.
  • Targeting fibrinogen represents a potential upstream therapeutic strategy to promote CNS repair in diseases characterized by remyelination failure.