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[FGF and physiopathological implications].

F Mascarelli1, A Torriglia, G Soubrane

  • 1Unité de Rercherches Gérontologiques, INSERM U118, Paris.

Annales D'Endocrinologie
|January 1, 1991
PubMed
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Fibroblast Growth Factor (FGF) plays a dual role in retinal diseases, acting as both a cause and potential therapy. Research shows FGF signaling defects contribute to retinal degeneration in RCS rats, impacting photoreceptor survival.

Area of Science:

  • Ophthalmology and Vision Science
  • Cell Biology
  • Molecular Genetics

Context:

  • Retinal pathologies, particularly those affecting photoreceptors (PR), are often linked to genetic defects.
  • The Royal College of Surgeons (RCS) rat model exhibits retinal degeneration due to a defect in retinal pigment epithelial (RPE) cells.
  • Fibroblast Growth Factor (FGF) has a demonstrated dual role in retinal conditions, acting as both a potential causative agent and a therapeutic agent.

Purpose:

  • To investigate the role of FGF signaling in the pathogenesis of retinal degeneration in the RCS rat model.
  • To compare FGF receptor (FGF-R) characteristics in dystrophic RCS rats versus normal sighted controls.
  • To elucidate the underlying molecular mechanisms of FGF action in retinal health and disease.

Summary:

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  • Studies on RCS rats revealed that transocular injection of FGF can reduce photoreceptor cell loss, highlighting its neuroprotective potential.
  • Analysis of purified RPE cells from RCS rats showed a significant reduction (approximately 70%) in cell surface FGF receptor number compared to controls, with similar affinities.
  • Defects in the FGF/FGF-R regulatory system are implicated as a potential cause of retinal degeneration in the RCS rat model, although in vivo mechanisms remain incompletely understood.

Impact:

  • Identifies a specific molecular defect in FGF receptor expression contributing to retinal dystrophy.
  • Provides a basis for exploring FGF-based therapeutic strategies for inherited retinal degenerations.
  • Underscores the need for further research into the complex in vivo mechanisms of FGF signaling in the retina.