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Eiichi Sato, Akira Takamiya, Atsushi Takahashi, Shinji Ono, Shinichi Otani, Chiemi Matsumoto, Akitoshi Yoshida; Plasma pentosidine and esRAGE concentrations in patients with age-related macular degeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2378.
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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.
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.
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.
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.
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