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Decidualization Resistance
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Irene Muñoz-Blat, Nerea Castillo-Marco, Teresa Cordero, Carlos Simón, Tamara Garrido-Gómez
The endometrial cycle has two dominant phases: the proliferative phase that follows menstruation and precedes ovulation, and the secretory phase characterized by the transformation into being receptive to embryo adhesion and differentiation to regulate embryo invasion (1) (Figure 23.1a). Following ovulation, estradiol induces increased progesterone receptor expression in stromal cells. Consequently, cells become responsive to progesterone and a coordinated cascade of modifications occurs in the tissue, leading to decidualization (2,3). Decidualization is a differentiation process of the endometrial cells in response to a hormonal stimulus released before pregnancy and is essential to a successful reproductive outcome. Curiously, in humans, decidualization occurs each menstrual cycle, regardless of whether implantation occurs (1).
The twentieth century
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
Based on Sampson’s original observation that pregnancy had a beneficial effect on endometriosis, R.W. Kistner (1958) reported on 58 cases treated by inducing pseudopregnancy with ovarian hormones. (Endometriotic tissue may possess estrogen, progesterone and androgen receptors.) Symptomatic improvement was presumed to be due to the decidualization and atrophy of implanted endometrial tissue. Pseudopregnancy remained as a popular therapy for endometriosis throughout the 1970s and was effected by oral or injectable progesterones. Cyclical therapy with the combined oral contraceptive pill was also thought to be helpful.
Prolactin Secretion in Neoplastic and Non-Neoplastic Uterine Lesions
Published in Nagasawa Hiroshi, Prolactin and Lesions in Breast, Uterus, and Prostate, 2020
A. Volpe, D. Campanin, F. Boselli
The initiation of PRL production by the endometrium coincides with the onset of its histological decidualization. Decidual cells release PRL, whereas no PRL was detectable in cultures of isolated epithelial endometrial cells.6 In women, decidualization begins under the influence of steroid hormones during the last week of the normal menstrual cycle, even in the absence of conception.7 This process begins around the spiral arteries on postovulatory day 9 and spreads through the stroma of the endometrium by the postovulatory day 13. Failure of the endometrium to undergo a normal decidual reaction during the last 6 days of the menstrual cycle is characteristic of luteal phase defect. Samples of luteal phase defect endometrium produced significantly less PRL than did control tissue of the same ideal menstrual dates.8
Progress of oxidative stress in endometrium decidualization
Published in Journal of Obstetrics and Gynaecology, 2022
Wenxin Gao, Fei Feng, Xiaoling Ma, Rui Zhang, Lifei Li, Feng Yue, Meng Lv, Lin Liu
Decidualization of human endometrium plays a key role in the establishment of pregnancy. In a narrow sense, endometrial decidualization means that ESCs begin to proliferate and differentiate into large and round multinucleated cells with rich cytoplasm. Generalised endometrial decidualization is based on the decidualization of ESCs, which occurs the secretion of endometrial glandular epithelial cells, the remodelling of spiral arteries and the recruitment and differentiation of immune cells (Sang et al.2020). In addition to the morphological changes in ESCs, there are changes in signal molecules in decidual cells, in which insulin-like growth factor binding protein 1 (IGFBP1) and prolactin (PRL) are classic markers of decidualization of ESCs (Ochiai et al.2019). Unlike most mammals, decidualization of the human uterus doesn’t depend on embryo implantation. After ovulation, the levels of progesterone and local cyclic adenosine monophosphate (cAMP) increase, which induces spontaneous decidualization. When the embryo doesn’t implant, the endometrium exfoliates and forms menstruation, with the decrease of hormone level (Evans et al.2016). If the embryo implants, decidualization is more intense, protecting the embryo from immune rejection (Ramathal et al.2010).
Placenta accrete after a frozen-thawed embryo transfer in a systemic lupus erythematosus patient treated with hydroxychloroquine
Published in Gynecological Endocrinology, 2020
Kazuki Saito, Chihiro Mano, Takayuki Tatsumi, Tomonori Ishikawa, Masaki Sekiguchi, Yuki Iwahara, Shiro Hiramitsu, Naoyuki Miyasaka
PA refers to abnormal placental attachment to the uterine wall, which is characterized by the invasion of trophoblasts into the myometrium [9]. Traditionally, PA is thought to be associated with defective decidualization because total or partial absence of decidua is the characteristic histological feature of PA. Uterine injury (i.e. previous endometrial curettage or cesarean section) is a known risk factor for PA, and defective decidualization is often observed in cases of implantation on uterine scars. Several other factors are possibly associated with defective decidualization. During the peri-implantation period, human endometrial stromal cells are decidualized in response to progesterone produced from the corpus luteum. Therefore, altered levels of progesterone possibly lead to abnormal placentation. In this regard, we had previously reported that endometrial preparation with artificial cycle for FET is strongly associated with PA [2]. Since the corpus luteum does not exist during an artificial cycle, the level of progesterone is maintained by hormonal supplementation until the placenta produces enough progesterone. Therefore, blood or local levels of progesterone might be insufficient, and the risk of PA is possibly increased in some cases. In addition, adrenal and ovarian steroidogenesis are suppressed in patients with SLE using immunosuppressive agents, such as prednisolone [6,10]. Therefore, hormonal insufficiency caused by inadequate hormonal replacement could be more remarkable in these patients.
New insight into the role of long non-coding RNAs in the pathogenesis of preeclampsia
Published in Hypertension in Pregnancy, 2019
Mohammad-Taher Moradi, Zohreh Rahimi, Asad Vaisi-Raygani
Abnormal placentation and uteroplacental circulation along with endothelial cell dysfunction are known risk factors involved in the pathogenesis of preeclampsia (7,13). Excessive apoptosis of trophoblast cells, poor invasion of the uterine wall by trophoblasts and impaired remodeling of spiral arteries at the maternal-fetal interface are major abnormal placentation events that are closely related to preeclampsia (14). Also, defects in decidualization may play a role in the pathogenesis of preeclampsia (15,16). Decidualization that is a process of endometrial stromal cell proliferation and differentiation is essential for implantation and maintenance of pregnancy. This process can regulate the invasion of extravillous trophoblast cells, remodeling of the uterine spiral artery, and finally placental formation (17). Furthermore, it is declared that successful pregnancy, similar to an allograft, needs maternal immune tolerance to the fetus; and PE is related to an imbalance of maternal immune tolerance. The local immune balance of the maternal-fetal interface has a tendency toward an inflammatory response which is dominated by T helper 1 (Th1) cells. Probably, over-maturation of dendritic cells in the decidua can stimulate differentiation of CD4+T cells into Th1 cells (18).