Epigenetics of Estrogen and Progesterone Receptors in Endometriosis
- PDF / 547,162 Bytes
- 8 Pages / 595.276 x 790.866 pts Page_size
- 38 Downloads / 173 Views
REVIEW
Epigenetics of Estrogen and Progesterone Receptors in Endometriosis Huixi Chen 1,2,3 & Francesca Malentacchi 1 & Massimiliano Fambrini 1 & Abdel Halim Harrath 4 & Hefeng Huang 2,3 & Felice Petraglia 1 Received: 24 March 2020 / Accepted: 25 May 2020 # Society for Reproductive Investigation 2020
Abstract Endometriosis is an estrogen-dependent inflammatory gynecological disease. Increased estrogen activity and progesterone resistance are the main hormonal substrate of this disease and are associated with inflammatory response and debilitating symptoms, including pain and infertility. Estrogens and progesterone act via their specific nuclear receptors. The regulation of receptor expression by epigenetics maybe a critical factor for endometriosis. The present review aims to discuss the epigenetic mechanisms related to the expression of estrogen receptors (ERs) and progesterone receptors (PRs) in patients with endometriosis, including two classic epigenetic mechanisms: DNA methylation and histone modification, and, other non-classic mechanisms: miRNAs and lncRNA. Several in vitro and in vivo studies support the key role of epigenetics in the regulation of the expression of ERs and PRs, which may provide new molecules and targets for the diagnosis and treatment of endometriosis. Keywords Estrogen receptor . Progesterone receptor . DNA methylation . Histone modification . miRNA . lncRNA
Introduction Endometriosis is a chronic estrogen-dependent and inflammatory gynecological disease which is characterized by presence of endometrial-like glands and stromal cells outside the uterus with debilitating symptoms including chronic pelvic pain and infertility [1, 2]. It was estimated to affect approximately 10% of women in reproductive age and up to 40% of women with infertility. The main etiopathogenic hypotheses of endometriosis include retrograde menstruation, coelomic metaplasia, and embryonic origin. Mechanisms involved in this complex and multifactorial disease include estrogen dependence,
* Felice Petraglia [email protected] 1
Obstetrics and Gynecology Unit, Department of Biomedical, Experimental and Clinical Sciences, University of Florence, Florence, Italy
2
International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
3
Shanghai Key Laboratory of Embryo Original Disease, Shanghai, China
4
Department of Zoology, College of Science, King Said University, Riyadh, Saudi Arabia
aberrant inflammatory response, angiogenesis abnormalities, genetic alterations, and epigenetic alterations [3]. As mentioned above, endometriosis is influenced by estrogen and progesterone. Estrogen plays a key role in promoting endometriotic tissue survival, cell proliferation, and inflammatory response [4]. Progesterone resistance [5] is associated with the development and progression of endometriotic lesions and with symptoms including chronic pelvic pain and infertility. Estrogen and progesterone act through specific receptors: estrogen receptor α (ERα), estro
Data Loading...
