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Fibulin-3 knockout mice demonstrate corneal dysfunction but maintain normal retinal integrity.

Steffi Daniel1, Marian Renwick1, Viet Q Chau1

  • 1Department of Ophthalmology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, USA.

Journal of Molecular Medicine (Berlin, Germany)
|September 23, 2020
PubMed
Summary

Fibulin-3 (F3) is crucial for corneal integrity but not essential for retinal or RPE function. Its absence in mice and humans shows potential for safe therapeutic strategies targeting eye diseases like AMD.

Keywords:
Age-related macular degeneration (AMD)CorneaEFEMP1Fibulin-3Malattia Leventinese (ML)Retina

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Area of Science:

  • Ophthalmology
  • Extracellular Matrix Biology
  • Genetics

Background:

  • Fibulin-3 (F3) is an extracellular matrix glycoprotein implicated in eye diseases.
  • A mutation in F3 causes macular dystrophy, and its absence protects mice from sub-retinal pigment epithelium (RPE) deposits.
  • The precise role of wild-type (WT) F3 in ocular tissues remains largely unknown.

Purpose of the Study:

  • To investigate the tissue-specific expression and function of Fibulin-3 (F3) within the eye.
  • To characterize the structural and functional consequences of F3 absence in ocular tissues.
  • To evaluate the potential of F3 as a therapeutic target for retinal diseases.

Main Methods:

  • Analysis of F3 expression across various mouse ocular tissues.
  • Structural and functional evaluation of ocular tissues in WT and F3 knockout (F3-/-) mice.
  • Utilized SD-OCT, histology, electron microscopy, electroretinogram, and optokinetic response tests.

Main Results:

  • F3 knockout mice exhibit progressive corneal thinning, opacity, and vascularization with age.
  • No significant structural or functional abnormalities were observed in the trabecular meshwork, neural retina, RPE, or optic nerve of F3-/- mice.
  • Absence of F3 in a human patient with loss-of-function mutations showed no retinal abnormalities.

Conclusions:

  • Fibulin-3 is essential for maintaining corneal structural integrity.
  • The absence of F3 does not compromise the structure or function of other ocular tissues, including the retina and RPE.
  • Targeted F3 inhibition presents a potentially safe therapeutic strategy for reducing sub-RPE deposits in diseases like age-related macular degeneration (AMD).