4.7 Article

Adenosine triphosphate-binding cassette transporter G2 expression in endometriosis and in endometrium from patients with and without endometriosis

Journal

FERTILITY AND STERILITY
Volume 98, Issue 6, Pages 1512-+

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.fertnstert.2012.07.1133

Keywords

ATP-binding cassette transporter G2; endometriosis; endometrium; microvessel

Funding

  1. Karl Storz Endoscopy & GmbH (Tuttlingen, Germany)

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Objective: To investigate adenosine triphosphate (ATP)-binding cassette transporter G2 (ABCG2) expression in endometriosis and in samples of endometrium from patients with and without endometriosis. Design: Prospective study. Setting: University hospital. Patient(s): Patients with and without endometriosis. Intervention(s): Endometrial and endometriotic tissues obtained throughout the menstrual cycle. Main Outcome Measure(s): Density of ABCG2(+) microvessels, density of CD31(+) microvessels. Result(s): No statistically significant differences in the density of ABCG2(+) microvessels were observed between endometrium of patients with and without endometriosis in the proliferative phase and early, middle, and late secretory phases. The density of ABCG2(+) microvessels was statistically significantly higher in the menstrual endometrium of patients with endometriosis compared with patients without endometriosis. The density of ABCG2(+) microvessels was reduced in the ectopic endometrium compared with matched eutopic endometrium except in cases of deep infiltrating endometriosis. The density of ABCG2(+) microvessels was statistically significantly higher in deep infiltrating endometriosis compared with ovarian endometriosis and red and black peritoneal lesions throughout the menstrual cycle. Conclusion(s): ABCG2 is strongly expressed in the endothelial cells of microvessels of eutopic endometrium, and the density of ABCG2(+) microvessels is reduced in ectopic endometrium except in cases of deep infiltrating endometriosis. ABCG2(+) microvessels may represent an integral part of the pathophysiology of deep infiltrating endometriosis. (Fertil Steril (R) 2012; 98: 1512-20. (C) 2012 by American Society for Reproductive Medicine.)

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