Progesterone resistance in endometriosis is modulated by the altered expression of microRNA-29c and FKBP4

Asgerally T. Fazleabas, P. Serafini, Eduardo Hideki Miyadahira, Yalda Afshar, Steven L. Young, Niraj Joshi, Bruce A. Lessey, Jae-Wook Jeong
2020 · doi:10.17615/h6k0-pt92 · W4298408900
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Increased miR-29c expression in endometriosis endometrium decreases FKBP4 levels, potentially causing progesterone resistance, which is reversed postoperatively.

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The paper studied how progesterone resistance in endometriosis is regulated, focusing on microRNA-29c (miR-29c) and its target FKBP4 in the eutopic endometrium. Using miR-expression analyses in a baboon endometriosis model and endometrial samples from women with deep infiltrative endometriosis versus controls, the authors found increased miR-29c expression in endometriosis and decreased FKBP4 transcript levels, while decidual markers were also reduced. They further supported a causal link by transfecting human uterine fibroblasts with a miR-29c mimic, which lowered FKBP4 mRNA and decidualization-associated markers. A key limitation acknowledged by the study design is that mechanistic evidence in humans relies on tissue correlations and in vitro fibroblast transfection rather than direct demonstration in vivo. This paper is centrally about endometriosis — specifically miR-29c–mediated modulation of FKBP4 contributing to progesterone resistance in eutopic endometrium.

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Abstract

Context: Endometriosis results in aberrant gene expression in the eutopic endometrium (EuE) and subsequent progesterone resistance. MicroRNA (miR) microarray data in a baboon model of endometriosis showed an increased expression of miR-29c. Objectives: To explore the role of miR-29c in progesterone resistance in a subset of women with endometriosis. Design: MiR-29c expression was analyzed in the endometrium of baboons and women with or without endometriosis. The role in progesterone resistance and decidualization was analyzed by transfecting human uterine fibroblast cells with miR-29c. Patients: Subjects diagnosed with deep infiltrative endometriosis (DIE) by transvaginal ultrasound with bowel preparation underwent surgical excision of endometriosis. Eutopic secretory endometrium was collected pre- and postoperatively. Women with normal EuE and without DIE served as controls. Results: Quantitative reverse transcription polymerase chain reaction demonstrated that miR-29c expression increased, while the transcript levels of its target, FK506-binding protein 4 (FKBP4), decreased in the EuE of baboons following the induction of endometriosis. FKBP4 messenger RNA and decidual markers were statistically significantly decreased in decidualized human uterine fibroblast cells transfected with a miR-29c mimic compared with controls. Human data corroborated our baboon data and demonstrated higher expression of miR-29c in endometriosis EuE compared with normal EuE. MiR-29c was significantly decreased in endometriosis EuE postoperatively compared with preoperative tissues, and FKBP4 showed an inverse trend following radical laparoscopic resection surgery. Conclusions: We demonstrate that miR-29c expression is increased in EuE of baboons and women with endometriosis, which might contribute to a compromised progesterone response by diminishing the levels of FKBP4. Resection of DIE is likely to reverse the progesterone resistance associated with endometriosis in women.
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Progesterone resistance in endometriosis is modulated by the altered expression of microRNA-29c and FKBP4 Public DepositedAdd to collection You do not have access to any existing collections. You may create a new collection. Downloadable Content Download PDFCitation MLA Joshi, Niraj R, et al. Progesterone Resistance In Endometriosis Is Modulated by the Altered Expression of Microrna-29c and Fkbp4. 2016. https://doi.org/10.17615/h6k0-pt92APA Joshi, N., Miyadahira, E., Afshar, Y., Jeong, J., Young, S., Lessey, B., Serafini, P., & Fazleabas, A. (2016). Progesterone resistance in endometriosis is modulated by the altered expression of microRNA-29c and FKBP4. https://doi.org/10.17615/h6k0-pt92Chicago Joshi, Niraj R., Eduardo H Miyadahira, Yalda Afshar, Jae Wook Jeong, Steven L Young, Bruce A Lessey, Paulo C Serafini et al. 2016. Progesterone Resistance In Endometriosis Is Modulated by the Altered Expression of Microrna-29c and Fkbp4. https://doi.org/10.17615/h6k0-pt92- Creator - Joshi, Niraj R. - Other Affiliation: Department of Obstetrics; Gynecology and Reproductive Biology; Michigan State University - Miyadahira, Eduardo H. - Other Affiliation: Huntigton Medicina Reprodutiva - Afshar, Yalda - Other Affiliation: Department of Obstetrics and Gynecology; University of California - Jeong, Jae-Wook - Other Affiliation: Department of Obstetrics; Gynecology and Reproductive Biology; Michigan State University - Young, Steven L. - School of Medicine, Department of Obstetrics and Gynecology - Lessey, Bruce A. - Other Affiliation: Greenville Hospital System; University of South Carolina; School of Medicine - Serafini, Paulo C. - Other Affiliation: Discipline of Gynecology; Department of Obstetrics and Gynecology; Hospital das Clinicas; Faculdade de Medicina; Universidade de São Paulo - Fazleabas, Asgerally T. - Other Affiliation: Department of Obstetrics; Gynecology and Reproductive Biology; Michigan State University - Joshi, Niraj R. - Abstract - Context: Endometriosis results in aberrant gene expression in the eutopic endometrium (EuE) and subsequent progesterone resistance. MicroRNA (miR) microarray data in a baboon model of endometriosis showed an increased expression of miR-29c. Objectives: To explore the role of miR-29c in progesterone resistance in a subset of women with endometriosis. Design: MiR-29c expression was analyzed in the endometrium of baboons and women with or without endometriosis. The role in progesterone resistance and decidualization was analyzed by transfecting human uterine fibroblast cells with miR-29c. Patients: Subjects diagnosed with deep infiltrative endometriosis (DIE) by transvaginal ultrasound with bowel preparation underwent surgical excision of endometriosis. Eutopic secretory endometrium was collected pre- and postoperatively. Women with normal EuE and without DIE served as controls. Results: Quantitative reverse transcription polymerase chain reaction demonstrated that miR-29c expression increased, while the transcript levels of its target, FK506-binding protein 4 (FKBP4), decreased in the EuE of baboons following the induction of endometriosis. FKBP4 messenger RNA and decidual markers were statistically significantly decreased in decidualized human uterine fibroblast cells transfected with a miR-29c mimic compared with controls. Human data corroborated our baboon data and demonstrated higher expression of miR-29c in endometriosis EuE compared with normal EuE. MiR-29c was significantly decreased in endometriosis EuE postoperatively compared with preoperative tissues, and FKBP4 showed an inverse trend following radical laparoscopic resection surgery. Conclusions: We demonstrate that miR-29c expression is increased in EuE of baboons and women with endometriosis, which might contribute to a compromised progesterone response by diminishing the levels of FKBP4. Resection of DIE is likely to reverse the progesterone resistance associated with endometriosis in women. - Date of publication - 2016 - Keyword - DOI - Identifier - PMID: 27778641 - PMCID: PMC5413101 - Onescience id: 62db1b51f1c087a708c7ec5791b8b271793d454b - Publisher DOI: https://doi.org/10.1210/jc.2016-2076 - Resource type - Article - Rights statement - In Copyright - Journal title - Journal of Clinical Endocrinology & Metabolism - Page start - jc.2016-2076 - Language - English - ISSN - 1945-7197 - 0021-972X Relations - Parents: This work has no parents. Items | Thumbnail | Title | Date Uploaded | Visibility | Actions | |---|---|---|---|---| | jc.2016-2076.pdf | 2016 | Public | Download |

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