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Concentrations of Receptor for Advanced Glycation End Products, VEGF and CML in Plasma, Follicular Fluid, and Peritoneal Fluid in Women With and Without Endometriosis

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Abstract

The etiology and pathogenesis of endometriosis is largely unknown. It has been reported that advanced glycation end products—receptor for advanced glycation end products regulation relates to oxidative stress, inflammatory reaction, apoptosis, and angiogenesis through vascular endothelial growth factor activation. The purpose of this study was to examine whether advanced glycation end products—receptor for advanced glycation end products regulation contributes to the pathogenesis of endometriosis. Plasma, follicular, and peritoneal fluid samples were collected from women with or without endometriosis, and soluble receptor for advanced glycation end products, vascular endothelial growth factor and carboxymethyl lysine levels were measured by enzyme-linked immunosorbent assay. Vascular endothelial growth factor and soluble receptor for advanced glycation end products concentrations were similar in plasma; however, their concentrations in follicular fluid were significantly increased in endometriosis patients (soluble receptor for advanced glycation end products was 132 + 31 pg/mg of protein vs. 105 + 27 pg/mg; vascular endothelial growth factor was 70 + 3 pg/mg vs. 49 + 18 pg/mg, expressed as the mean + standard deviation). Increased soluble receptor for advanced glycation end products and vascular endothelial growth factor levels in a local environment suggest that the advanced glycation end products—receptor for advanced glycation end products may contribute to the pathogenesis of endometriosis.

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Correspondence to Eriko Y. Fujii MD, PhD.

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The study was supported by the Ministry of Health, Labour and Welfare research expense, Policy consignment 17–6, Japan.

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Fujii, E.Y., Nakayama, M. & Nakagawa, A. Concentrations of Receptor for Advanced Glycation End Products, VEGF and CML in Plasma, Follicular Fluid, and Peritoneal Fluid in Women With and Without Endometriosis. Reprod. Sci. 15, 1066–1074 (2008). https://doi.org/10.1177/1933719108323445

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