Modulation of SOD3 Levels Is Detrimental to Retinal Homeostasis

Antioxidants

Muayyad R. Al-Ubaidi¹  Muna I. Naash¹  Larissa Ikelle¹ 

[1] Department of Biomedical Engineering, University of Houston, Houston, TX 77004, USA;

关键词: retina;    extracellular matrix;    oxidative stress;    SOD3;    retinal degeneration;    superoxide dismutase 3;   

DOI  :  10.3390/antiox10101595

来源: DOAJ

【 摘 要 】

Retinal oxidative stress is a common secondary feature of many retinal diseases. Though it may not be the initial insult, it is a major contributor to the pathogenesis of highly prevalent retinal dystrophic diseases like macular degeneration, diabetic retinopathy, and retinitis pigmentosa. We explored the role of superoxide dismutase 3 (SOD3) in retinal homeostasis since SOD3 protects the extracellular matrix (ECM) from oxidative injury. We show that SOD3 is mainly extracellularly localized and is upregulated as a result of environmental and pathogenic stress. Ablation of SOD3 resulted in reduced functional electroretinographic responses and number of photoreceptors, which is exacerbated with age. By contrast, overexpression showed increased electroretinographic responses and increased number of photoreceptors at young ages, but appears deleterious as the animal ages, as determined from the associated functional decline. Our exploration shows that SOD3 is vital to retinal homeostasis but its levels are tightly regulated. This suggests that SOD3 augmentation to combat oxidative stress during retinal degenerative changes may only be effective in the short-term.

【 授权许可】

Unknown