Protein kinase C activation and calcium mobilization decrease prolactin release from human decidual cells in early pregnancy

Kubota, Toshiro; Kamada, Shinji; Taguchi, Makoto; Sakamoto, S.; Asô, Takeshi

doi:10.1677/joe.0.1370335

Cited by 6 publications

(2 citation statements)

References 20 publications

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“…The release of prolactin, at least in the short term, is not dependent on alterations in Ca + (Sartor et al 1992). In contrast, phorbol esters via protein kinase C (Kubota et al 1993), cytokines except interleukin-6 (Jikihara and lipopolysaccharides (Chao et al 1994) all inhibited prolactin secretion by term decidua in culture. All these in vitro studies suggest mechan¬ isms which may interact in a paracrine or autocrine manner to regulate prolactin production by the decidua.…”

Section: Discussionmentioning

confidence: 88%

The relationship between decidualization and prolactin mRNA and production at different stages of human pregnancy

Wen¹,

Brooks²,

Glasier³

et al. 1995

Journal of Molecular Endocrinology

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Within the human utero-placental unit only decidualized stromal cells express mRNA for prolactin. However, it is not clear if the level of prolactin production is related to the number of decidualized cells or the capacity of individual decidual cells to synthesize prolactin, either or both of which parameters may change during pregnancy. In the present study, prolactin production at different stages of human pregnancy was examined using quantitative in situ hybridization to assess decidual prolactin mRNA abundance, immunocytochemistry to examine the prolactin content inside decidual cells and RIA to measure decidual prolactin output into amniotic fluid. Throughout pregnancy the proportion of stromal cells showing positive immunostaining and mRNA for prolactin increased. There was a parallel increase in decidual cell size which was correlated with an increase in prolactin gene expression and intensity of immunostaining for prolactin in individual decidual cells. These changes in decidual cells were consistent with the changes in the concentration of prolactin in amniotic fluid. These results suggest that there is a close link between the level of prolactin gene expression and production of prolactin by individual decidual cells, which in turn is directly related to the process of decidualization that continues throughout human pregnancy.

show abstract

Section: Discussionmentioning

confidence: 88%

The relationship between decidualization and prolactin mRNA and production at different stages of human pregnancy

Wen¹,

Brooks²,

Glasier³

et al. 1995

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…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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Early cell signaling by the cytotoxic enterotoxin of Aeromonas hydrophila in macrophages

Ribardo

Kuhl

Boldogh

et al. 2002

Microbial Pathogenesis

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Protein kinase C activation and calcium mobilization decrease prolactin release from human decidual cells in early pregnancy

Cited by 6 publications

References 20 publications

The relationship between decidualization and prolactin mRNA and production at different stages of human pregnancy

The relationship between decidualization and prolactin mRNA and production at different stages of human pregnancy

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

Early cell signaling by the cytotoxic enterotoxin of Aeromonas hydrophila in macrophages

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