Abstract
Purpose:
Advanced glycation end products (AGEs) have been implicated in the pathogenesis of age-related macular degeneration (AMD) through binding to their receptor, RAGE. However, endogenous secretory RAGE (esRAGE) captures AGEs and protects against AGE-induced effects. In the current study, we investigated the relationship between plasma pentosidine (a well-defined AGE) and plasma esRAGE and wet AMD.
Methods:
Thirty-one patients with wet AMD and 15 control subjects (age range, 58~90 years) were included. Of the patients with wet AMD, 10 had typical AMD and 21 had polypoidal choroidal vasculopathy (PCV). A commercially available competitive enzyme-linked immunosorbent assay was used to measure the plasma pentosidine and esRAGE concentrations in the patients with AMD and the control subjects.
Results:
The plasma pentosidine level in typical AMD (mean ± standard deviation, 0.125 ± 0.0210 µg/mL) was significantly (P < 0.05) higher than in the control subjects (0.0245 ± 0.0153 µg/mL) and the patients with PCV (0.0221 ± 0.0202 µg/mL). Although the esRAGE level in the patients with PCV (0.177 ± 0.0991 ng/mL) tended to be lower than in the control subjects (0.241 ± 0.0918 ng/mL) and in the patients with typical AMD (0.259 ± 0.134 ng/mL), the plasma esRAGE levels did not differ significantly among the groups.
Conclusions:
Our results suggested that increased pentosidine levels may be implicated in the pathogenesis of typical AMD, but systemic levels of circulating esRAGE may not be associated with wet AMD.