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Related Experiment Video

Updated: Jan 10, 2026

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects
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FOXP2-Dependent Vulnerability of RGCs Under Acute Ocular Hypertension.

Meifang Yan1, Junjian Li1, Zihao Zhang1

  • 1State Key Laboratory of Ophthalmology, Optometry and Visual Science, Eye Hospital, Wenzhou Medical University, 270 Xueyuan Road, Wenzhou, Zhejiang, 325027, P. R. China.

Molecular Neurobiology
|November 22, 2025
PubMed
Summary

The gene Foxp2 increases retinal ganglion cell vulnerability to ocular hypertension (OHT) in glaucoma. Reducing Foxp2 expression protects these cells by improving axonal transport.

Keywords:
Foxp2Axonal transportGlaucomaOcular hypertensionRetinal ganglion cells

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Genetics

Background:

  • Glaucoma involves elevated intraocular pressure (IOP), damaging the optic nerve and retinal ganglion cells (RGCs).
  • RGC subtypes show varied susceptibility to ocular hypertension (OHT).
  • The role of Foxp2 in RGC vulnerability during OHT is unexplored.

Purpose of the Study:

  • Investigate the relationship between RGC selective vulnerability and the gene Foxp2 in OHT.
  • Determine if Foxp2 influences RGC damage and axonal transport under OHT conditions.

Main Methods:

  • Induced acute OHT in mice.
  • Assessed RGC apoptosis and survival, focusing on FOXP2-positive RGCs (F-RGCs).
  • Performed retina-specific Foxp2 knockout (KO) and analyzed RGC axon integrity and retrograde transport.

Main Results:

  • Acute OHT increased RGC apoptosis and disproportionately reduced F-RGCs.
  • Retina-specific Foxp2 KO mitigated RGC loss and axon degeneration caused by OHT.
  • F-RGCs exhibited higher dynactin-1 expression and slower axonal transport, suggesting impaired dynactin/dynein function.

Conclusions:

  • Foxp2 contributes to RGC vulnerability in OHT, potentially by slowing axoplasmic transport.
  • Targeting Foxp2 or its downstream pathways may offer neuroprotective strategies for glaucoma.