Dynamic expression of PGRMC1 and SERBP1 in human endometrium: an implication in the human decidualization process

Salsano, Stefania; Quiñonero, Alicia; Pérez, Silvia; Garrido-Gómez, Tamara; Simón, Carlos; Domı́nguez, Francisco

doi:10.1016/j.fertnstert.2017.07.1163

Cited by 25 publications

(23 citation statements)

References 53 publications

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“…PGRMCs are encoded by two genes, PGRMC1 and PGRMC2, and their expression was originally discovered in rat and porcine hepatocytes (77, 78). Since then, PGRMC1 has been isolated from a range of human cells and tissues, including neuronal, breast, and reproductive tissues (62, 79–81), and have been found to localize to both the plasma membrane and organelle membranes (82–85). The ability of PGRMC1 to bind to P4 has been demonstrated with the use of radioactive P4 ligand binding measurements from porcine liver membrane fractions and, more recently, spectroscopy (77, 86).…”

Section: Receptor-mediated Actionsmentioning

confidence: 99%

Progesterone-Related Immune Modulation of Pregnancy and Labor

et al. 2019

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Pregnancy involves a complex interplay between maternal neuroendocrine and immunological systems in order to establish and sustain a growing fetus. It is thought that the uterus at pregnancy transitions from quiescent to laboring state in response to interactions between maternal and fetal systems at least partly via altered neuroendocrine signaling. Progesterone (P4) is a vital hormone in maternal reproductive tissues and immune cells during pregnancy. As such, P4 is widely used in clinical interventions to improve the chance of embryo implantation, as well as reduce the risk of miscarriage and premature labor. Here we review research to date that focus on the pathways through which P4 mediates its actions on both the maternal reproductive and immune system. We will dissect the role of P4 as a modulator of inflammation, both systemic and intrinsic to the uterus, during human pregnancy and labor.

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Section: Receptor-mediated Actionsmentioning

confidence: 99%

Progesterone-Related Immune Modulation of Pregnancy and Labor

et al. 2019

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“…This pathway could be physiologically important because many of the actions of P 4 occur too rapidly to be explained by changes in gene and/or protein expression (90). Uterine epithelial cell PGRMC1 content in macaques and humans was higher during the proliferative than the secretory phase of menstrual cycles (91,92). Ablation of Pgrmc1 from the mouse uterus reduced litter sizes 40% without affecting the ability of the animals to ovulate (90).…”

Section: Insr Mrna Expression In Response To E 2 P 4 and Insulinmentioning

confidence: 99%

Glycogen metabolism in mink uterine epithelial cells and its regulation by estradiol, progesterone and insulin

et al. 2019

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Glycogen content in mink uterine glandular and luminal epithelia (GE and LE) is maximal during estrus and is depleted before implantation while embryos are in diapause. Uterine glycogen synthesis in vivo is stimulated by estradiol (E 2 ) while its mobilization is induced by progesterone (P 4 ). Nevertheless, treatment of an immortalized mink uterine epithelial cell line (GMMe) with E 2 did not affect glycogen production. Interestingly, insulin alone significantly increased synthesis of the nutrient and glycogen content in response to insulin + E 2 was greater than for insulin alone. Our objectives were to determine: 1) If insulin receptor protein (INSR) is expressed by mink uterine GE and LE in vivo and if the amount differs between estrus, diapause and pregnancy; 2) if E 2 , P 4 or insulin regulate insulin receptor gene (Insr) expression by GMMe cells, and 3) if E 2 and P 4 act independently to regulate glycogen metabolism by GMMe cells and/or if their effects are mediated in part through the actions of insulin. The mean (±S.E.) ±percent INSR content of uterine epithelia was greatest during diapause (GE: 15.65±0.06, LE:16.56±1.25), much less during pregnancy (GE: 2.53±0.60, LE:2.25±0.32) and barely detectable in estrus (GE: 0.03±0.01, LE: 0.02±0.01). Glycogen concentrations in GMMe cells increased 10-fold in response to insulin and 20-fold with insulin+E 2 when compared to controls. Expression of Insr was increased 2-fold by insulin and insulin+E 2 when compared to controls and there was no difference between the two hormone treatments, indicating that E 2 does not increase Insr expression in insulin-treated cells.To simulate E 2 -priming, cells were treated with Insulin + E 2 for 24 h, followed by the same hormones + P 4 for the second 24 h (Insulin+E 2 → P 4 ) which resulted in Insr and glycogen levels not different from controls. Similarly, cells treated with Insulin+P 4 resulted in glycogen concentrations not different from controls. We conclude that the glycogenic actions of E 2 on GMMe cells are due to increased responsiveness of the cells to insulin, but not as a result of upregulation of the insulin receptor. Glycogen mobilization in response to P 4 was the result of decreased glycogenesis and increased glycogenolysis occurring concomitantly with reduced Insr expression. Mink uterine glycogen metabolism appears to be regulated in a reproductive cycle-*

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“…Because PGRMC1 was predominantly found expressed in stromal cells as opposed to epithelial cells in the mid-secretory phase, it was initially presumed that it was a critical regulator of decidualization. In the past year, a more convincing study demonstrated that overexpression of PGRMC1 in stromal cells compromised in-vitro-induced decidualization as manifested by attenuated PRL synthesis and absence of typical morphological features [ 103 ]. Notably, the authors have previously discovered the PGRMC1 protein to be one of the few differentially expressed between receptive and nonreceptive endometrium [ 104 ].…”

Section: Decidualization Route: Priming the Endometrium For Implanmentioning

confidence: 99%

Inside the Endometrial Cell Signaling Subway: Mind the Gap(s)

Makieva

Giacomini

Ottolina

et al. 2018

IJMS

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Endometrial cells perceive and respond to their microenvironment forming the basis of endometrial homeostasis. Errors in endometrial cell signaling are responsible for a wide spectrum of endometrial pathologies ranging from infertility to cancer. Intensive research over the years has been decoding the sophisticated molecular means by which endometrial cells communicate to each other and with the embryo. The objective of this review is to provide the scientific community with the first overview of key endometrial cell signaling pathways operating throughout the menstrual cycle. On this basis, a comprehensive and critical assessment of the literature was performed to provide the tools for the authorship of this narrative review summarizing the pivotal components and signaling cascades operating during seven endometrial cell fate “routes”: proliferation, decidualization, implantation, migration, breakdown, regeneration, and angiogenesis. Albeit schematically presented as separate transit routes in a subway network and narrated in a distinct fashion, the majority of the time these routes overlap or occur simultaneously within endometrial cells. This review facilitates identification of novel trajectories of research in endometrial cellular communication and signaling. The meticulous study of endometrial signaling pathways potentiates both the discovery of novel therapeutic targets to tackle disease and vanguard fertility approaches.

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Dynamic expression of PGRMC1 and SERBP1 in human endometrium: an implication in the human decidualization process

Abstract: Our results suggest that classic P receptors (PRs) are not the only kind playing a role in the normal physiology of the endometrium. The human decidualization process could be altered by the overexpression or mislocalization of PGRMC1 in ESC.

Cited by 25 publications

References 53 publications

Progesterone-Related Immune Modulation of Pregnancy and Labor

Progesterone-Related Immune Modulation of Pregnancy and Labor

Glycogen metabolism in mink uterine epithelial cells and its regulation by estradiol, progesterone and insulin

Inside the Endometrial Cell Signaling Subway: Mind the Gap(s)

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