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Related Experiment Video

Updated: Nov 2, 2025

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
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Elevated Hydrostatic Pressure Causes Retinal Degeneration Through Upregulating Lipocalin-2.

Azusa Yoneshige1, Man Hagiyama1, Yasutoshi Takashima1

  • 1Department of Pathology, Faculty of Medicine, Kindai University, Osaka, Japan.

Frontiers in Cell and Developmental Biology
|June 17, 2021
PubMed
Summary

Increased eye pressure elevates Lipocalin 2 (Lcn2) in retinal cells, causing neurotoxicity and cell death. This study shows Lcn2 directly contributes to glaucoma-like damage, suggesting Lcn2 and iron modulation as potential therapies.

Keywords:
apoptosisglaucomagliosisintraocular pressureiron chelatorretinal ganglion cells

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Cell Biology

Background:

  • Elevated intraocular pressure is a primary risk factor for glaucoma, leading to retinal ganglion cell (RGC) loss.
  • Lipocalin 2 (Lcn2) is found in increased levels in glaucomatous retinae, but its direct role remains unclear.

Purpose of the Study:

  • To investigate the direct role of Lipocalin 2 (Lcn2) in retinal degeneration caused by elevated hydrostatic pressure.
  • To determine if Lcn2 contributes to RGC apoptosis and gliosis under increased intraocular pressure conditions.

Main Methods:

  • Retinal explant cultures were subjected to increased hydrostatic pressure (50 cm H2O vs. 20 cm H2O) using a two-chamber system.
  • Lcn2 protein levels were measured by immunoblotting; apoptosis and gliosis were assessed using TUNEL and GFAP assays, respectively.
  • Neurotoxicity of Lcn2 was evaluated by exogenous administration, and the effect of iron chelation was tested using deferoxamine.

Main Results:

  • Elevated hydrostatic pressure significantly increased Lcn2 protein levels, RGC apoptosis (TUNEL-positive cells), and gliosis (GFAP-positive area).
  • Exogenous Lcn2 demonstrated dose-dependent neurotoxicity in retinal explants (1 μg/ml).
  • The detrimental effects of increased pressure were mitigated by the iron chelator deferoxamine.

Conclusions:

  • This study provides the first evidence that elevated hydrostatic pressure directly upregulates Lcn2 in the retina.
  • Lcn2 contributes to pressure-induced retinal neurodegeneration, highlighting its potential as a therapeutic target.
  • Modulating Lcn2 and iron levels may offer a novel strategy for treating retinal degeneration in glaucoma.