Background/Aims: Oxidative stress that damages cells of the retinal pigment epithelium (RPE) can cause the development of hereditary retinal disease (HRD). PRDX6, which is a member of the PRDX family, is essential for removing metabolic free radicals from the body. However, the effect of PRDX6 on oxidative stress in HRD remains unknown. In this study, we sought to investigate the role of PRDX6 in oxidative stress-induced HRD in ARPE-19 cells and the molecular mechanism involved. Methods: ARPE-19 cells were used in the current study. Intracellular ROS levels were determined by flow cytometry. Lipid peroxidation was measured using a commercial MDA assay kit. Cellular variability was determined by MTT assay. Apoptosis was determined using an Annexin V-FITC Apoptosis Detection Kit. mRNA and protein expression levels were detected by real-time PCR and western blot analysis, respectively. Results: We found that H₂O₂ and blue light could induce significant oxidative stress damage and cell death in ARPE-19 cells. Furthermore, we found that PRDX6 levels significantly decreased after H₂O₂ treatment. PRDX6 overexpression protected ARPE-19 cells from H₂O₂- and blue light-induced oxidative damage, while PRDX6 knockdown enhanced oxidative damage in these cells. Mechanistically, we found that PRDX6 prevented oxidative damage and promoted ARPE-19 cell survival through the PI3K/AKT signaling pathway. Conclusions: Collectively, these results suggest that PRDX6 protects ARPE-19 cells from H₂O₂-induced oxidative stress and apoptosis and that this protection is mediated at least partially through the PI3K/AKT pathway.

No abstract

Immunoglobin (IgG4)-related disease in the eye and ocular adnexa (IgG4-ROD) is a newly discovered autoimmune disease that histologically exhibits extensive lymphocyte and plasma cell infiltration, occlusive phlebitis and mat or whorled fibrosis. The disease can affect multiple ocular tissues and organs, such as the lacrimal gland, extraocular muscles, orbital fat and trigeminal nerve. The main clinical manifestations are chronic, painless swelling of the orbit or unilateral orbit and proptosis, which may be accompanied by peripheral lymphadenopathy. Usually, visual impairment is not apparent, but in severe cases, it can cause a loss of function of the tissues and organs involved and affect the daily lives of patients. The pathogenesis of IgG4-ROD is not clear. Based on existing literature, it is speculated that it may be related to factors such as autoantibody production, microbial infection and genetic inheritance. For the treatment of IgG4-ROD, glucocorticoids, immunosuppressive agents, biological agents and surgery are mainly used in clinical practice. Although these treatment methods can achieve a particular effect, they have limitations, such as high recurrence rates, serious side effects and postoperative complications. With the increase in IgG4-ROD-related reports, some progress has been made in the current understanding and research of the disease.

Hereditary retinal disease (HRD) is the primary retinal degeneration that leads to severe visual impairments and refractory blindness, and the therapy of HRD was most important in ophthalmology. The apoptosis of retinal cells plays important roles in HRD progression. Therefore, in this study, we explore the mechanism of H2O2 and blue light-induced apoptosis of ARPE-19 cells. Co-immunoprecipitation (Co-IP) is employed to test the interactions between proteins, and western blotting is used to detect the protein levels. Apoptosis is analyzed by Flow cytometry. Our results found that PRDX6 could interact with RARA in ARPE-19 cells, and H2O2 and blue light could significantly reduce the RARA protein expression, and also could inhibit the interaction between PRDX6 and RARA. Using a rescue experiment, we further elucidated that H2O2 and blue light reduced the RARA expression via down-regulating PRDX6. And H2O2 and blue light induced the ARPE-19 cell apoptosis via decreasing the expression of PRDX6. Our results suggested that the interaction between PRDX6 and RARA played important roles in the apoptosis of ARPE-19 cells.