http://nova.newcastle.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5059 Phytoestrogens may function as partial agonists or antagonists of estrogen in many tissues including bone. Five phytoestrogens, belonging to the isoflavones and the flavonoids groups, were assayed in the human MG-63 osteoblastic cell line for their ability to stimulate transcriptional activity of an estrogen-response element (ERE)-luciferase reporter gene via the estrogen receptor β (ERβ). Although MG-63 cells were shown to express endogenous estrogen receptors, estradiol (E₂) did not affect transcriptional activity of an ERE reporter in these cells. However, E₂ did activate the ERE-reporter significantly in MG-63 cells where ERβ was overexpressed. The isoflavones, genistein and daidzein, caused a dose-dependent increase in the ERE-reporter activity in MG-63 cells overexpressing ERβ. Among the flavonoids, kaempferol activated ERE-reporter activity, whereas puerarin inhibited ERE-reporter transcription in cells overexpressing ERβ. Quercetin had no effect on ERE-reporter activity over a concentration range of 10⁻¹⁰–10⁻⁶ mol/l. The ERE-reporter activity induced by daidzein, genistein, and kaempferol was blocked by both ICI 182780 and 4-hydroxytamoxifen and partly blocked by puerarin. Our results demonstrated that different phytoestrogens exhibited differential transcription activity of an ERE-reporter via ERβ-mediated mechanisms in MG-63 cells. 2010-04-27T04:35:13.107Z ]]> http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5295 Placental corticotropin-releasing hormone (CRH) plays an important role in the mechanisms controlling human pregnancy and parturition, and several endogenous factors are known to regulate placental CRH gene expression. In this article, the authors investigate the regulation of the CRH gene’s promoter activity by a protein kinase C (PKC) activator, phorbol-12-myristate-13-acetate (PMA), in primary cultures of placental cells. The PMA stimulation of the CRH gene promoter activity was dose dependent, and further studies, including progressive deletion and mutation analysis of the CRH promoter, localized the region essential for PMA responsiveness to a consensus cyclic adenosine monophosphate regulatory element (CRE). Furthermore, estradiol treatment resulted in decreases of both basal and PMA-stimulated promoter activity when the CRE element was present but had no effect when the CRE element was absent. Thus, PMA stimulates CRH gene transcriptional activity through the CRE, suggesting that cross-talk between PKC and protein kinase A signaling pathways targets this regulatory element in placental cells. 2010-04-27T04:33:16.708Z ]]>