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Endometrial progesterone receptor isoforms in women with polycystic ovary syndrome

Journal article
Authors Min Hu
Juan Li
Yuehui Zhang
Xin Li
Mats Brännström
Linus Ruijin Shao
Håkan Billig
Published in American Journal of Translational Research
Volume 10
Issue 8
Pages 2696–2705
ISSN 1943-8141
Publication year 2018
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 2696–2705
Language en
Links https://www.ncbi.nlm.nih.gov/pmc/ar...
https://www.researchgate.net/public...
www.ajtr.org/files/ajtr0073905.pdf
Keywords Progesterone receptor isoforms, estrogen receptor, hyperandrogenism, endometrium, PCOS, infertility
Subject categories Clinical Laboratory Medicine, Obstetrics and women's diseases, Endocrinology

Abstract

Context: Polycystic ovary syndrome (PCOS) affects approximately 4%-18% of all reproductive-aged women and is often accompanied by endometrial progesterone (P4) resistance. Endometrial cells from PCOS patients display increased progesterone receptor (PGR) expression; however, in vivo knockout studies and in vitro experiments indicate the two PGR isoforms are not functionally equivalent. Objective: We aimed to compare endometrial PGR iso-form expression between non-PCOS and PCOS patients during the proliferative phase. Design: A case-control study. The expression of PGR isoforms (PGRA and PGRB), estrogen receptor alpha (ERα), and markers of cell proliferation was determined by qRT-PCR, Western blot, immunohistochemistry, and immunofluorescence assays. Patient(s): Patients were recruited and diagnosed with PCOS according to the Rotterdam criteria provided by the American Society for Reproductive Medicine and the European Society for Human Reproduction and Embryology. Endometrial biopsy samples were collected from non-PCOS patients with regular menstrual cycles or with hyperplasia (n = 11) and from PCOS patients with or without hyperplasia (n = 14). Result(s): Although the alteration of PGRB mRNA and protein expression was different, we found that PGRA mRNA and protein expression was higher in PCOS patients than non-PCOS patients. PGRA/B and PGRB were localized in both epithelial and stromal cells, with notable changes in the nuclei of epithelial and stromal cells. A similar expression pattern of ERα, vimentin and Ki-67, in association with an increased PGR expression, was observed in PCOS patients. Conclusion(s): These results demonstrated that elevated both PGR isoform expression depends on the presence of PCOS, and our data suggest that abnormal regulation of PGR isoforms is a pathological outcome of defective endometrium in PCOS patients.

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