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OTX2 Non-Cell Autonomous Activity Regulates Inner Retinal Function.

Raoul Torero Ibad1, Bilal Mazhar1, Clémentine Vincent1

  • 1Centre for Interdisciplinary Research in Biology (CIRB), Collège de France, CNRS, UMR 7241, INSERM U1050, Labex MemoLife, Université PSL (Paris Sciences & Lettres), 75005 Paris, France.

Eneuro
|August 2, 2020
PubMed
Summary
This summary is machine-generated.

Extracellular OTX2 (orthodenticle homeobox 2) promotes retinal cell survival. Neutralizing extracellular OTX2 in mice reduced visual acuity and altered inner retinal function.

Keywords:
homeoprotein non-cell autonomousphysiology retinavision

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Genetics

Background:

  • OTX2 is a homeoprotein transcription factor crucial for retinal development.
  • It exhibits non-cell autonomous activity, influencing cells beyond its expression site.
  • Retinal ganglion cell survival is promoted by extracellular OTX2.

Purpose of the Study:

  • To investigate the role of extracellular OTX2 in postnatal retinal function.
  • To assess the impact of neutralizing OTX2's non-cell autonomous activity in vivo.

Main Methods:

  • Genetic targeting of extracellular OTX2 using a secreted single-chain anti-OTX2 antibody in mice.
  • Assessment of visual acuity, retinal structure, and cell types.
  • Electrophysiological recordings (electroretinogram) to evaluate retinal function.

Main Results:

  • Expression of the anti-OTX2 antibody led to reduced visual acuity in 1-month-old mice.
  • No significant alterations in retinal structure or cell populations were observed.
  • Electroretinogram showed no deficits in photoreceptor or bipolar cell function, but altered inner retinal function.

Conclusions:

  • Interfering with extracellular OTX2 activity in the postnatal retina impacts inner retinal function.
  • Non-cell autonomous OTX2 activity is critical for maintaining normal visual acuity.
  • Targeting extracellular OTX2 offers a potential avenue for understanding and treating visual deficits.