Follicle-Stimulating Hormone Receptor Expression in Endometriotic Lesions and the Associated Vasculature: An Immunohistochemical Study

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This study found robust follicle-stimulating hormone receptor vascular expression in all tested endometriotic lesions, with varying expression in glandular and stromal cells, differing from normal endometrium.

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This immunohistochemical study assessed follicle-stimulating hormone receptor (FSHR) expression in 194 archival tissue specimens representing rectovaginal endometriotic nodules, ovarian endometriotic cysts, and peritoneal endometriotic implants, using normal endometrium as controls and a monoclonal antihuman FSHR antibody. Robust FSHR expression was consistently detected in blood vessels across all endometriosis lesion locations, while FSHR was not detected in normal host tissues located more than 5 mm from lesions, and endometriotic lymphatic vessels showed no FSHR expression; the density of FSHR-positive vessels was higher in rectovaginal nodule cores than in adjacent tissue, and FSHR was also detected in endometriotic glandular epithelial cells and/or stromal cells in roughly one-fifth to one-quarter of patients. A caveat is that tissue was examined from different lesion types and locations without an explicit functional or mechanistic assessment of how FSHR expression influences lesion biology. This paper is centrally about endometriosis — it characterizes FSHR expression in endometriotic lesions and their associated vasculature.

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Abstract

Follicle-stimulating hormone receptor (FSHR) is present on endothelial cells of blood vessels and endometrial glands of the proliferative and secretory endometrium. So far, the expression of FSHR in endometriosis has not been studied. We evaluated FSHR expression in 194 tissue specimens representing 3 relevant types of endometriosis: rectovaginal endometriotic nodules, ovarian endometriotic cysts, and peritoneal endometriotic implants. Specimens of normal endometrium were used as controls. Archival formalin-fixed and paraffin-embedded material was analyzed immunohistochemically with a highly specific monoclonal antihuman FSHR antibody using the peroxidase method. A robust vascular FSHR expression was found in all 194 patients, irrespective of the endometriosis lesion location. Follicle-stimulating hormone receptor was not detected in normal host tissues located more than 5 mm from the lesions. The endometriotic lymphatic vessels do not express FSHR. The density of FSHR-positive vessels in patients with rectovaginal endometriotic nodules was 46.0 ± 5.7 vessels/mm2. Similar values were obtained for ovarian endometriotic cysts and peritoneal endometriosis. The density of FSHR-positive vessels associated with the core of rectovaginal endometriotic nodules was 2-fold higher than that of the perilesional, adjacent normal host tissue (64.2 ± 8.2 vs 27.2 ± 3.2 vessels/mm2, respectively). Expression of FSHR was also detected either in endometriotic glandular epithelial cells, endometriotic stromal cells, or in both cell types (23%, 25%, and 21% of patients, respectively). Normal endometrium expressed FSHR predominately in basalis, in a cellular distribution dependent on hormonal environment. In conclusion, our data suggest novel FSHR expression in endometriotic lesions, qualitatively and quantitatively different from that of normal endometrium. Similar content being viewed by others

References

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endometriosis

MeSH descriptors

Blood Vessels Endometriosis Endometriosis Receptors, FSH Blood Vessels Endometriosis Endometrium Endometrium Endometrium Endometrium Endothelial Cells Endothelial Cells Female Humans Immunohistochemistry Receptors, FSH

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