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RXR Gamma Enables Oligodendrocyte Differentiation by Suppressing Sonic Hedgehog Signaling.

Vito Antonio Baldassarro1,2, Quentin Brassart1, Valérie Fraulob1

  • 1Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique UMR 7104, Institut national de la santé et de la recherche médicale U 1258, Illkirch, Université de Strasbourg, Strasbourg, France.

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|April 4, 2026
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Summary

Retinoid X receptor gamma (RXRg) is crucial for oligodendrocyte differentiation in multiple sclerosis therapy. Its absence causes SHH pathway hyperactivity, blocking remyelination, which can be reversed by inhibiting SHH signaling.

Keywords:
oligodendrocyte progenitorsoligodendrogenesisretinoid X receptorssonic hedgehogthyroid hormone

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Multiple sclerosis (MS) therapy aims to overcome remyelination failure.
  • Oligodendrocyte precursor cell (OPC) differentiation into myelinating oligodendrocytes (OLs) is key for remyelination.
  • Thyroid hormone, nuclear receptors, and sonic hedgehog (SHH) pathway regulate OPC differentiation.

Purpose of the Study:

  • Investigate the role and mechanism of Retinoid X receptor gamma (RXRg) in OPC differentiation and remyelination.
  • Determine RXRg's interaction with SHH signaling in the context of oligodendrocyte development.

Main Methods:

  • Transcriptomic and pharmacological analysis of primary neural stem cell-derived OPCs.
  • Utilized RXRg knockout (Rxrg-/-) and wild-type OPCs.
  • Employed SHH pathway modulators (cyclopamine, GANT61, purmorphamine, SAG).

Main Results:

  • RXRg promotes thyroid hormone-driven OPC differentiation and oligodendrogenic fate.
  • Loss of RXRg leads to upregulation of SHH signaling.
  • Inhibition of SHH signaling rescues differentiation and myelination deficits in Rxrg-/- OPCs.
  • SHH pathway hyperactivation inhibits OPC differentiation and myelination in wild-type cells.

Conclusions:

  • RXRg acts as a negative modulator of SHH signaling during OPC differentiation.
  • SHH pathway hyperactivity is a key factor in remyelination failure associated with RXRg absence.
  • Optimal fine-tuning of SHH signaling is essential for successful oligodendrogenesis and remyelination.