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E2 Treatment (e2 + treatment)
Selected AbstractsMorphine modulation of temporomandibular joint-responsive units in superficial laminae at the spinomedullary junction in female rats depends on estrogen statusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2008A. Tashiro Abstract The influence of analgesic agents on neurons activated by stimulation of the temporomandibular joint (TMJ) region is not well defined. The spinomedullary junction [trigeminal subnucleus caudalis (Vc)/C1,2] is a major site of termination for TMJ sensory afferents. To determine whether estrogen status influences opioid-induced modulation of TMJ units, the classical opioid analgesic, morphine, was given to ovariectomized (OvX) rats and OvX rats treated for 2 days with low-dose (LE2) or high-dose (HE2) 17,-estradiol-3-benzoate. Under thiopental anesthesia, TMJ units in superficial and deep laminae at the Vc/C1,2 junction were activated by injection of ATP (1 mm) directly into the joint space. In superficial laminae, morphine inhibited evoked activity in units from OvX and LE2 rats in a dose-related and naloxone-reversible manner, whereas units from HE2 rats were not inhibited. By contrast, in deep laminae, morphine reduced TMJ-evoked unit activity similarly in all groups. Morphine reduced the background activity of units in superficial and deep laminae and resting arterial pressure similarly in all groups. Morphine applied to the dorsal surface of the Vc/C1,2 junction inhibited all units independently of E2 treatment. Quantitative polymerase chain reaction and immunoblots revealed a similar level of expression for ,-opioid receptors at the Vc/C1,2 junction in LE2 and HE2 rats. These results indicated that estrogen status differentially affected morphine modulation of TMJ unit activity in superficial, but not deep, laminae at the Vc/C1,2 junction in female rats. The site(s) for estrogen influence on morphine-induced modulation of TMJ unit activity was probably outside the medullary dorsal horn. [source] Estrogen modulates estrogen receptor , and , expression, osteogenic activity, and apoptosis in mesenchymal stem cells (MSCs) of osteoporotic miceJOURNAL OF CELLULAR BIOCHEMISTRY, Issue S36 2001Shuanhu Zhou Abstract In the mouse, ovariectomy (OVX) leads to significant reductions in cancellous bone volume while estrogen (17,-estradiol, E2) replacement not only prevents bone loss but can increase bone formation. As the E2-dependent increase in bone formation would require the proliferation and differentiation of osteoblast precursors, we hypothesized that E2 regulates mesenchymal stem cells (MSCs) activity in mouse bone marrow. We therefore investigated proliferation, differentiation, apoptosis, and estrogen receptor (ER) , and , expression of primary culture MSCs isolated from OVX and sham-operated mice. MSCs, treated in vitro with 10,7 M E2, displayed a significant increase in ER, mRNA and protein expression as well as alkaline phosphatase (ALP) activity and proliferation rate. In contrast, E2 treatment resulted in a decrease in ER, mRNA and protein expression as well as apoptosis in both OVX and sham mice. E2 up-regulated the mRNA expression of osteogenic genes for ALP, collagen I, TGF-,1, BMP-2, and cbfa1 in MSCs. In a comparison of the relative mRNA expression and protein levels for two ER isoforms, ER, was the predominant form expressed in MSCs obtained from both OVX and sham-operated mice. Cumulatively, these results indicate that estrogen in vitro directly augments the proliferation and differentiation, ER, expression, osteogenic gene expression and, inhibits apoptosis and ER, expression in MSCs obtained from OVX and sham-operated mice. Co-expression of ER,, but not ER,, and osteogenic differentiation markers might indicate that ER, function as an activator and ER, function as a repressor in the osteogenic differentiation in MSCs. These results suggest that mouse MSCs are anabolic targets of estrogen action, via ER, activation. J. Cell. Biochem. Suppl. 36: 144,155, 2001. © 2001 Wiley-Liss, Inc. [source] Expression of RIZ1 protein (Retinoblastoma-interacting zinc-finger protein 1) in prostate cancer epithelial cells changes with cancer grade progression and is modulated in vitro by DHT and E2JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2009Valentina Rossi The nuclear protein methyl-transferase Retinoblastoma-interacting zinc-finger protein 1 (RIZ1) is considered to be a downstream effector of estrogen action in target tissues. Silencing of RIZ1 expression is common in many tumors. We analyzed RIZ1 expression in normal and malignant prostate tissue and evaluated whether estradiol (E2) or dihydrotestosterone (DHT) treatment modulated RIZ1 in cultured prostate epithelial cells (PEC). Moreover, we studied the possible involvement of RIZ1 in estrogen action on the EPN prostate cell line, constitutively expressing both estrogen receptor (ER)-, and ,. RIZ1 protein, found in the nucleus of normal PECs by immunohistochemistry, was progressively lost in cancer tissues as the Gleason score increased and was only detected in the cytoplasmic compartment. RIZ1 transcript levels, as assayed by semi-quantitative RT-PCR in primary PEC cultures, were significantly reduced in cancer cells (P,<,0.05). In EPN DHT treatment significantly increased RIZ1 transcript and protein levels (P,<,0.05); E2 induced a reduction of S phase without significant changes of RIZ1 expression. In E2-treated EPN cell extracts RIZ co-immunoprecipitated with ER, and ER,. Our data demonstrate that RIZ1 is expressed in normal PECs and down-regulated in cancer cells, with a switch of its sub-cellular localization from the nucleus to the cytoplasm upon cancer grade progression. RIZ1 expression levels in the PECs were modulated by DHT or E2 treatment in vitro. Furthermore, the E2 effects on ER-expressing prostate cells involve RIZ1, which confirms a possible role for ER-mediated pathways in a non-classic E2 -target tissue. J. Cell. Physiol. 221: 771,777, 2009. © 2009 Wiley-Liss, Inc. [source] Influence of plasma lipid changes in response to 17,-oestradiol stimulation on plasma growth hormone, somatostatin, and thyroid hormone levels in immature rainbow troutJOURNAL OF FISH BIOLOGY, Issue 3 2001F. Mercure Plasma total lipids were significantly higher in 17,-oestradiol(E2)-treated immature rainbow trout Oncorhynchus mykiss at week 4 after implantation, due to increases in polar and neutral lipids. The lipid classes responding were phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, sterols and sterol esters, in a proportion that approximately reflected the increase in plasma vitellogenin (VtG) levels as measured by a non-competitive enzyme-linked immunosorbent assay (ELISA). Plasma non-esterified fatty acids and triacylglycerol were not affected by E2 treatment. Plasma growth hormone GH levels were increased, and plasma somatostatin-14 (SRIF) levels decreased in E2 -treated fish, responses which could be secondary to elevated plasma lipid (VtG) content, although a direct E2 action on somatotroph function is possible. Plasma T4 concentrations were not affected by E2 treatment, but plasma T3 concentrations were significantly lower than in controls 1 week after implantation when plasma E2 concentrations were the highest; this is in support of the hypothesis that E2 has a suppressive action on T3 production. [source] Estrogen-mediated immunomodulation involves reduced activation of effector T cells, potentiation of treg cells, and enhanced expression of the PD-1 costimulatory pathwayJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2006Magdalena J. Polanczyk Abstract Estrogen (E2)-induced immunomodulation involves dual effects on antigen-presenting cells (APC) and CD4+CD25+ regulatory T cells (Treg) but not a direct effect on effector T cells. In this report, we further investigated the effects of E2 on APC and Treg function. We found that E2 treatment in vivo strongly reduced recovery of APC from the peritoneal cavity and inhibited induction of the inflammatory cytokines interleukin (IL)-12 and interferon-, but enhanced secretion of IL-10. Moreover, E2-conditioned bone marrow-derived dendritic cells (BM-DC) could both enhance Treg activity and directly inhibit responder T cells in the absence of Treg cells. We examined whether this E2-induced inhibitory activity of BM-DC might involve costimulation through the recently described PD-1 pathway. Both E2 and pregnancy markedly enhanced PD-1 expression in several types of APC, including macrophages, B cells, and especially dendritic cells (DC). Similarly to E2-induced enhancement of FoxP3 expression and experimental autoimmune encephalomyelitis protection, E2-induced enhancement of PD-1+ cells was also mediated through estrogen receptor alpha (Esr1) in DC and macrophages but not in B cells. Based on antibody inhibition studies, PD-1 interaction with its ligands, PDL-1 and especially PDL-2, could mediate either positive or negative regulatory signaling in both mature and immature E2-conditioned DC, depending, respectively, on a relatively high (10:1) or low (1:1) ratio of T cells:BM-DC. These novel findings indicate that E2-induced immunomodulation is mediated in part through potentiation in BM-DC of the PD-1 costimulatory pathway. © 2006 Wiley-Liss, Inc. [source] ORIGINAL ARTICLE: Effects of Cyclic Versus Sustained Estrogen Administration on Peripheral Immune Functions in Ovariectomized MiceAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Jing Li Citation Li J, McMurray RW. Effects of cyclic versus sustained estrogen administration on peripheral immune functions in ovariectomized mice. Am J Reprod Immunol 2010; 63: 274,281 Problem, Estrogens have multiple influences on immune functions. We aimed to compare the effects of cyclic versus sustained estrogen treatments under the same accumulated dose on peripheral immune functions in ovariectomized mice. Method of study, Ovariectomized adult Balb/c mice were treated with estradiol (E2) by s.c. injection once every 4 days (total 44.8 ,g) or by pellet implantation (total 44.2 ,g). After 6 weeks of treatment, all animals were immunized with DNP-KLH. Peripheral immune functions were assessed 10 days later. Results, Both cyclic and sustained E2 treatments significantly reduced the percentage of splenic B220+sIgM+ cells, enhanced IFN-, production and suppressed IL-6 secretion from Con A-stimulated splenocytes, and increased serum anti-DNP antibody levels. No differences were found in the above responses or in uterine weight gain between the two regimens of E2 administration. Conclusion, There are no differential effects on peripheral immune functions between cyclic and sustained estrogen administration under the same total dose. [source] | |||||||||||||||||||