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Sigma 1 Receptor Contributes to Astrocyte-Mediated Retinal Ganglion Cell Protection.

Jing Zhao1,2, Graydon B Gonsalvez3, Barbara A Mysona1,3,2

  • 1Department of Ophthalmology, Medical College of Georgia at Augusta University, Augusta, Georgia, United States.

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Sigma 1 receptor (S1R) in optic nerve head astrocytes supports retinal ganglion cell growth and survival. Its absence impairs neurite outgrowth and increases RGC apoptosis, suggesting a glia-mediated neuroprotective role.

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Cell Biology

Background:

  • Sigma 1 receptor (S1R) is known for its neuroprotective properties.
  • S1R is expressed in retinal ganglion cells (RGCs) and astrocytes.
  • Activation of S1R has demonstrated neuroprotective effects.

Purpose of the Study:

  • To investigate the specific role of S1R in optic nerve head astrocytes (ONHAs).
  • To determine the contribution of S1R in ONHAs to the growth and survival of RGCs in vitro.

Main Methods:

  • Cocultured wild-type (WT) RGCs with WT or S1R knockout (S1R KO) ONHAs for 2, 4, or 7 days.
  • Measured neurite length, root, and extremity counts; assessed RGC apoptosis via TUNEL assay.
  • Evaluated signal transducer and activator of transcription 3 (STAT3) phosphorylation levels in ONHAs.

Main Results:

  • Coculture with WT ONHAs promoted RGC neurite growth and survival compared to S1R KO ONHAs.
  • Absence of S1R in ONHAs led to decreased neurite length and increased RGC apoptosis.
  • S1R KO ONHAs exhibited reduced STAT3 phosphorylation compared to WT ONHAs.

Conclusions:

  • The absence of S1R in ONHAs negatively impacts RGC neurite growth and survival.
  • S1R in ONHAs appears to play a crucial role in maintaining RGC health.
  • Data suggest S1R enhances RGC survival through glia-mediated mechanisms.