Long-term effects of calcium availability on prolactin and protein synthesis in human decidual cells

Couderc, B.; Dufy-Barbe, L.; Sartor, P

doi:10.1016/s0143-4004(05)80004-9

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…This modulates the size of the releasable hormone pool via effects on cell protein synthesis mechanisms in general. To summarize, Ca 2ϩ leads to long-term dPRL release via acting on total protein synthesis rate but not on the specific modification of dPRL synthesis in human decidual cells (25).…”

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 90%

“…The contribution of calcium ions to successful decidualization is confirmed in mice (25). In the lectin-concanavalin A-induced (Con-A) pseudopregnant animals, Con A binds to epithelial surface glycoproteins and induces the production of a decidual response in the uterine lumen (108,109), which is undiscerning compared with that induced by blastocyst during implantation (107).…”

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 94%

“…So, longterm dPRL release is a key event for decidulization and implantation. Increasing external calcium ion concentrations does not induce the short-term secretion of dPRL in human decidual cells, but external calcium ions can produce their effects by promoting long-term release of dPRL (25). This modulates the size of the releasable hormone pool via effects on cell protein synthesis mechanisms in general.…”

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 99%

“…Luminal decidual cells synthesize and release decidual prolactin (dPRL), which is closely linked to the process of decidualization. As the marker of decidualization, it is responsible for the coordination of the establishment and maintenance of pregnancy via entry into the circulation or locally (cytokines) through juxtacrine, paracrine, and autocrine modes of action (25,50,113,126). So, longterm dPRL release is a key event for decidulization and implantation.…”

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 99%

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Ion/Water Channels for Embryo Implantation Barrier

et al. 2014

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Successful implantation involves three distinct processes, namely the embryo apposition, attachment, and penetration through the luminal epithelium of the endometrium to establish a vascular link to the mother. After penetration, stromal cells underlying the epithelium differentiate and surround the embryo to form the embryo implantation barrier, which blocks the passage of harmful substances to the embryo. Many ion/water channel proteins were found to be involved in the process of embryo implantation. First, ion/water channel proteins play their classical role in establishing a resting membrane potential, shaping action potentials and other electrical signals by gating the flow of ions across the cell membrane. Second, most of ion/water channel proteins are regulated by steroid hormone (estrogen or progesterone), which may have important implications to the embryo implantation. Last but not least, these proteins do not limit themselves as pure channels but also function as an initiator of a series of consequences once activated by their ligand/stimulator. Herein, we discuss these new insights in recent years about the contribution of ion/water channels to the embryo implantation barrier construction during early pregnancy.

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Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 90%

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 94%

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 99%

Section: Calcium Calcium Channels Calcium Transporter and Binding Pmentioning

confidence: 99%

See 2 more Smart Citations

Ion/Water Channels for Embryo Implantation Barrier

et al. 2014

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“…It was previously shown that the treatment with Ca 2+ ionophore A23187 attenuates prolactin release in decidual cells prepared from patients in early pregnancy [ 25 ], and that Ca 2+ channel blockers inhibit prolactin secretion in human decidual cells [ 26 ]. Ruan et al .…”

Section: Discussionmentioning

confidence: 99%

Regulatory Action of Calcium Ion on Cyclic AMP-Enhanced Expression of Implantation-Related Factors in Human Endometrial Cells

et al. 2015

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Decidualization of human endometrial stroma and gland development is mediated through cyclic AMP (cAMP), but the role of intracellular calcium ion (Ca2+) on cAMP mediated-signaling in human endometrial stroma and glandular epithelia has not been well-characterized. The present study was designed to investigate the role of intracellular Ca2+ on cAMP mediated-decidualization and gland maturation events, which can be identified by the up-regulation of prolactin and IGF-binding protein (IGFBP)1 in human endometrial stromal cells (ESCs), and cyclooxygenase 2 (COX2) and prostaglandin E2 (PGE2) and glandular epithelial EM-1 cells. Increases in decidual prolactin and IGFBP-1 transcript levels, induced by cAMP-elevating agents forskolin or dibutyryl cyclic AMP, were inhibited by Ca2+ influx into ESCs with Ca2+ ionophores (alamethicin, ionomycin) in a dose-dependent manner. Conversely, inhibitors of Ca2+ influx through L-type voltage-dependent Ca2+ channel (VDCC), nifedipine and verapamil, enhanced the decidual gene expression. Furthermore, dantrolene, an inhibitor of Ca2+ release from the intracellular Ca2+ store, up-regulated prolactin and IGFBP-1 expression. Ca2+ ionophores decreased intracellular cAMP concentrations, whereas nifedipine, verapamil or dantrolene increased cAMP concentrations in ESCs. In glandular epithelial cells, similar responses in COX2 expression and PGE2 production were found when intracellular cAMP levels were up-regulated by decreases in Ca2+ concentrations. Thus, a marked decrease in cytosolic Ca2+ levels caused the elevation of cAMP concentrations, resulting in enhanced expression of implantation-related factors including decidual markers. These findings suggest that fluctuation in cytosolic Ca2+ concentrations alters intracellular cAMP levels, which then regulate differentiation of endometrial stromal and glandular epithelial cells.

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