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

Capsule:
ABCG2 was strongly expressed in endothelial cells of microvessels of eutopic endometrium, and the density of ABCG2+ microvessels was reduced in ectopic endometrium except in cases of deep infiltrating endometriosis.

Authors:
Sachiko Matsuzaki, M.D. and Claude Darcha, M.D.

Volume 98, Issue 6, Pages 1512-1520.e3, December 2012

Abstract:

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.

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