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β-HCG/LH Receptor (β-HCG/LH-R) Expression in Eutopic Endometrium and Endometriotic Implants: Evidence for β-HCG Sensitivity of Endometriosis

Division of Special Gynaecology, Department of Obstetrics and Gynaecology, Medical University of Vienna, Department of Obstetrics and Gynaecology Worthing and Southlands Hospital, Worthing, UK

Ambros Huber, MD

Divisions of Obstetrics and Gynaecology, Medical University of cVienna

Martin Knoefler, MD

Divisions of Obstetrics and Gynaecology, Medical University of cVienna

Sandra Haider

Divisions of Obstetrics and Gynaecology, Medical University of cVienna

Andrea Kolbus, MD

Divisions of Gynaecological Endocrinology and Reproductive Medicine, Medical University of Vienna

Klaus Czerwenka, MD

Division of Gynaecopathology, Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria

Samir Helmy, MD

Division of Special Gynaecology, Department of Obstetrics and Gynaecology, Medical University of Vienna

Ernst Kubista, MD

Division of Special Gynaecology, Department of Obstetrics and Gynaecology, Medical University of Vienna

Christian F. Singer, MD, MPH

Division of Special Gynaecology, Department of Obstetrics and Gynaecology, Medical University of Vienna, christian.singer{at}meduniwien.ac.at

Background: Luteinizing hormone (LH) and human chorionic gonadotropin (HCG) target their receptor in gonadal and nongonadal cells to stimulate steroidogenesis and cell growth. The aim of the present study was to investigate the expression of HCG/LH-R in endometriosis to elucidate a possible impact of LH and HCG on this disease. Materials and methods: Analysis of HCG/LH-R protein expression in 23 paired samples of ectopic and eutopic tissue of cycling women with endometriosis and in endometrial samples from 22 healthy controls was conducted via immunofluorescence. HCG and HCG/LH-R gene expression in endometriotic lesions was confirmed by reverse-transcriptase polymerase chain reaction. Results: In endometriotic implants, epithelial HCG/LH-R was found in 12/23 samples. No significant differences in HCG/LH-R levels were observed when compared with glands of uterine endometrium from the same patients or healthy controls. Messenger RNA transcripts for HCG were detected in all 12 samples, whereas HCG/LH-R mRNAs were observed in 10 of the 12 endometriotic lesions investigated. Conclusions: Although HCG/LH-R was not found to be selectively upregulated in endometriosis, the mere presence of HCG/LH-R in endometriotic tissue may suggest sensitivity of endometriosis to HCG and LH that target HCG/LH-R.

Key Words: β-HCG-receptor • endometriosis • expression.

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