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Related Experiment Video

Updated: Jun 26, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

Published on: February 15, 2020

Oxidative stress promotes ocular neovascularization.

Aling Dong¹, Bing Xie, Jikui Shen

¹Departments of Ophthalmology and Neuroscience, Johns Hopkins, University School of Medicine, Baltimore, Maryland, USA.

Journal of Cellular Physiology

|January 15, 2009

Summary

Mice lacking superoxide dismutase 1 (SOD1) show increased ocular neovascularization (NV). Antioxidant treatment reduced NV in these mice and wild-type mice, suggesting reactive oxygen species drive NV development.

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Last Updated: Jun 26, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage

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Visualization of Vascular Ca²⁺ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

Area of Science:

Ocular biology
Vascular biology
Age-related macular degeneration (AMD) research

Background:

Superoxide dismutase 1 (SOD1) deficiency in mice mimics features of age-related macular degeneration (AMD), including choroidal neovascularization (NV).
The role of SOD1 deficiency in creating a pro-angiogenic subretinal environment is unclear, potentially being secondary to other retinal changes.

Purpose of the Study:

To investigate whether SOD1 deficiency directly contributes to a pro-angiogenic environment in the subretinal space.
To determine if the absence of SOD1 exacerbates neovascularization in ocular disease models.

Main Methods:

Comparison of neovascularization in Sod1(-/-) mice versus Sod1(+/+) mice in ischemic retinopathy and VEGF-driven transgenic models.
Assessment of the effects of antioxidant treatment on retinal and choroidal NV in Sod1(-/-) and wild-type mice.

Main Results:

Sod1(-/-) mice exhibited significantly more NV in both ischemic and VEGF-driven models compared to Sod1(+/+) mice.
Antioxidant treatment markedly reduced ischemia-induced retinal NV in Sod1(-/-) mice.
Antioxidants also reduced NV in wild-type mice, including ischemia-induced, VEGF-induced subretinal, and choroidal NV.

Conclusions:

The compromised antioxidant defense in Sod1(-/-) mice contributes to a pro-angiogenic environment, promoting ocular NV.
Reactive oxygen species (ROS) play a significant role in various forms of ocular NV.
These findings support the potential therapeutic benefit of potent antioxidants for AMD and other conditions involving ocular NV.