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Presence and synthesis of inhibin subunits in human decidua.
No full textA growing number of studies provided the evidence that human decidua is a pregnancy-related tissue capable of hormone production and metabolism. The aim of the present study was to evaluate the possible presence of inhibin subunits in human decidua. Tissue samples were collected in pregnant women during the first (8 weeks) and second trimester (18 weeks) of gestation and at term (40 weeks). Immunohistochemical data were obtained using affinity purified polyclonal antisera raised in rabbit against porcine alpha, beta A, or beta B subunits. Levels of the respective inhibin subunits were evaluated by Northern blot analysis using cDNA probes encoding sequences corresponding to each subunit. The present results indicated that human decidua contains and synthesizes inhibin alpha, beta A, and beta B subunits. The immunohistochemical data showed that decidual cells were stained with both inhibin alpha and beta B antisera, showing a similar localization. On the other hand, cells stained with inhibin beta A antisera were sparse and followed a distribution pattern different from that of cells stained with alpha or beta B antisera. The first inhibin alpha and beta B subunit mRNAs were both expressed in first trimester of pregnancy, and those mRNA levels showed a gestational related increase. The beta A subunit mRNA was expressed at very low levels at term and could not be detected earlier during pregnancy. The present data showed that human decidua actively produces inhibin subunits with a gestational-related profile. The results suggest that decidua may be a further source of inhibin-related proteins during pregnancy and emphasize the endocrine competence of human decidua
Mechanism of action of interleukin-1 beta in increasing corticotropin-releasing factor and adrenocorticotropin hormone release from cultured human placental cells.
No full textThe present study evaluated the possible effect and mechanism of action of interleukin-1 beta in regulating the release of corticotropin-releasing factor and adrenocorticotropin hormone from human cultured placental cells. With the use of a primary monolayer culture of human placental cells at term, the addition of interleukin-1 beta increased the release of immunoreactive corticotropin-releasing factor with a dose- and time-dependent effect. The intracellular concentration of both cyclic adenosine monophosphate and cyclic guanosine monophosphate increased in the presence of interleukin-1 beta. The addition of indomethacin, a prostaglandin synthesis inhibitor, partially reversed the effect of interleukin-1 beta. The same doses of interleukin-1 beta stimulated the release of adrenocorticotropin hormone and this effect was partially reversed by the addition of a synthetic corticotropin-releasing factor antagonist or by indomethacin. This study showed that interleukin-1 beta increases the release of corticotropin-releasing factor and adrenocorticotropin hormone from cultured placental cells. This effect is associated with increased intracellular cyclic nucleotide concentrations and is in part reversed by a prostaglandin synthesis inhibitor
Mechanism of action of interleukin-1 beta in increasing corticotropin-releasing factor and adrenocorticotropin hormone release from cultured human placental cells.
No full textThe present study evaluated the possible effect and mechanism of action of interleukin-1 beta in regulating the release of corticotropin-releasing factor and adrenocorticotropin hormone from human cultured placental cells. With the use of a primary monolayer culture of human placental cells at term, the addition of interleukin-1 beta increased the release of immunoreactive corticotropin-releasing factor with a dose- and time-dependent effect. The intracellular concentration of both cyclic adenosine monophosphate and cyclic guanosine monophosphate increased in the presence of interleukin-1 beta. The addition of indomethacin, a prostaglandin synthesis inhibitor, partially reversed the effect of interleukin-1 beta. The same doses of interleukin-1 beta stimulated the release of adrenocorticotropin hormone and this effect was partially reversed by the addition of a synthetic corticotropin-releasing factor antagonist or by indomethacin. This study showed that interleukin-1 beta increases the release of corticotropin-releasing factor and adrenocorticotropin hormone from cultured placental cells. This effect is associated with increased intracellular cyclic nucleotide concentrations and is in part reversed by a prostaglandin synthesis inhibitor
Human decidua and in vitro decidualized endometrial stromal cells produce corticotropin-releasing factor: changes of mRNA levels during pregnancy
No full textHuman decidua and in vitro decidualized endometrial stromal cells at term contain immunoreactive corticotropin-releasing factor (CRF) and CRF messenger ribonucleic acid.
No full textCRF, a hypothalamic neurohormone, has been shown to be present in several tissues outside the brain. During pregnancy, both fetal (placental trophoblast, chorion, and amnion) and maternal (decidua) intrauterine tissues contain immunoreactive CRF. A paracrine/autocrine role of CRF as a regulator of hormonogenesis in human placenta and decidua has been suggested. The expression of CRF mRNA in human decidua was demonstrated in the present study by Northern blot analysis and was found to be higher in specimens collected at term than in those collected during the first and second trimesters of gestation. Furthermore, the presence of CRF was detected immunocytochemically in cultured decidual cells isolated from term decidua as well as in endometrial stromal cells decidualized in vitro by treatment with a mixture of medroxyprogesterone acetate, estradiol, and relaxin. These results indicate that human decidua is an intrauterine extrahypothalamic source of CRF in the maternal compartment and offer new tools to explore the in vitro decidualization processes and the regulation of CRF release from decidual cells
Presenza di mRNA del Corticotropin-releasinng factor (CRF) nella decidua e nel trofoblasto umano
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