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Oestradiol Treatment (oestradiol + treatment)
Selected AbstractsStroke Injury in Rats Causes an Increase in Activin A Gene Expression Which is Unaffected by Oestradiol TreatmentJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2006M. Böttner Abstract Activins are members of the transforming growth factor-, superfamily that exert neurotrophic and neuroprotective effects on various neuronal populations. To determine the possible function of activin in stroke injury, we assessed which components of the activin signalling pathway were modulated in response to middle cerebral artery occlusion (MCAO). Furthermore, because oestradiol replacement protects against MCAO-induced cell death, we explored whether oestradiol replacement influences activin gene expression. Female Sprague-Dawley rats underwent permanent MCAO and the expression of activins and their corresponding receptors was determined by semiquantitative reverse transcriptase-polymerase chain reaction at 24 h after onset of ischaemia. We observed up-regulation of activin ,A and activin type I receptor A mRNA in response to injury. Dual-label immunocytochemistry followed by confocal z-stack analysis showed that the activin A expressing cells comprised neurones. Next, we monitored the time course of activin ,A mRNA expression in oestradiol- or vehicle-treated rats at 4, 8, 16 and 24 h after MCAO via in situ hybridisation. Starting at 4 h after injury, activin ,A mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin ,A mRNA levels in the cortex increased dramatically with time and were highest at 24 h after the insult, and oestradiol replacement did not influence this increase. [source] Double Oestrogen Receptor , and , Knockout Mice Reveal Differences in Neural Oestrogen-Mediated Progestin Receptor Induction and Female Sexual BehaviourJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2003A. E. Kudwa Abstract To test the hypothesis that oestrogen receptor , (ER,) and ER, act together to mediate the actions of oestrogen in the ventromedial hypothalamus (VMH), we used mice with single or double knockout mutations of the ER, and ER, genes. Ovariectomized mice were implanted with 17,-oestradiol and killed 5 days later. Oestradiol treatment promoted progestin receptor (PR)-immunoreactivity (-ir) in the VMH of all genotypes, but was maximal in brains of wild-type and ER,KO females. Analysis of specific VMH subregions revealed that PR-ir induction was limited to the caudal VMH in ER,KO and ER,,KO mice. In the rostral VMH, oestradiol only induced PR-ir in wild-type and ER,KO mice, and the number of PR-ir neurones in this region was greater in ER,KO than wild-type females. Next, we tested the ability of a dopamine agonist and progesterone to facilitate sexual behaviour in females lacking functional ER,, ER,, or both receptors. Ovariectomized mice were implanted with oestradiol, and tested for sexual behaviour three times after administration of the dopamine agonist, apomorphine, followed by two tests concurrent with progesterone treatment and a final test with just apomorphine treatment. ER,KO and ER,,KO females failed to display lordosis under any testing conditions, while ER,KO females exhibited lordosis behaviour equal to that of wild-type females. Our data show that a subpopulation of PR-ir neurones is induced by oestradiol in the caudal VMH of female mice lacking both ER, and ER, genes. We hypothesize that this action of oestradiol is either mediated by a novel ER or by the mutant portion of the AF2 subregion of the ER, gene present in ER,KO brain. However, despite the presence of PR in VMH, females lacking a functional ER, gene do not display sexual behaviour, via either ligand-dependent or -independent activation. [source] Tissue-specific regulation of ACE/ACE2 and AT1/AT2 receptor gene expression by oestrogen in apolipoprotein E/oestrogen receptor-, knock-out miceEXPERIMENTAL PHYSIOLOGY, Issue 5 2008K. Bridget Brosnihan Angiotensin-converting enzyme (ACE) and ACE2 and the AT1 and AT2 receptors are pivotal points of regulation in the renin,angiotensin system. ACE and ACE2 are key enzymes in the formation and degradation of angiotensin II (Ang II) and angiotensin-(1,7)(Ang-(1,7)). Ang II acts at either the AT1 or the AT2 receptor to mediate opposing actions of vasoconstriction or vasodilatation respectively. While it is known that oestrogen acts to downregulate ACE and the AT1 receptor, its regulation of ACE2 and the AT2 receptor and the involvement of a specific oestrogen receptor subtype are unknown. To investigate the role of oestrogen receptor-, (ER,) in the regulation by oestrogen of ACE/ACE2 and AT1/AT2 mRNAs in lung and kidney, ovariectomized female mice lacking apolipoprotein E (ee) with the ER, (AAee) or without the ER, (,,ee) were treated with 17,-oestradiol (6 ,g day,1) or placebo for 3 months. ACE, ACE2, AT1 receptor and AT2 receptor mRNAs were measured using reverse transcriptase, real-time polymerase chain reaction. In the kidney, 17,-oestradiol showed 1.7-fold downregulation of ACE mRNA in AAee mice, with 2.1-fold upregulation of ACE mRNA in ,,ee mice. 17,-Oestradiol showed 1.5- and 1.8-fold downregulation of ACE2 and AT1 receptor mRNA in AAee mice; this regulation was lost in ,,ee mice. 17,-Oestradiol showed marked (81-fold) upregulation of the AT2 receptor mRNA in AAee mice. In the lung, 17,-oestradiol treatment had no effect on AT1 receptor mRNA in AAee mice, but resulted in a 1.5-fold decreased regulation of AT1 mRNA in ,,ee mice. There was no significant interaction of oestrogen with ER, in the lung for ACE, ACE2 and AT2 receptor genes. These studies reveal tissue-specific regulation by 17,-oestradiol of ACE/ACE2 and AT1/AT2 receptor genes, with the ER, receptor being primarily responsible for the regulation of kidney ACE2, AT1 receptor and AT2 receptor genes. [source] Oestradiol Induced Inhibition of Neuroendocrine Marker Expression in Leydig Cells of Adult RatsREPRODUCTION IN DOMESTIC ANIMALS, Issue 3 2006HH Ortega Contents The objectives of this work were to determine the changes in the expression of neuroendocrine markers in Leydig cell by oestradiol treatment, and to determine whether testosterone is able to recover partially the effects of hormonal suppression induced by oestradiol. Adult male rats were injected daily with either 50 ,g of oestradiol or oestradiol plus testosterone propionate (25 mg every 3 days) for 15 days. The animals were sacrificed and testicles were dissected and processed by routine histological protocols. FSH and LH serum levels were determined by radioimmunoassay. The visualization of antigens was achieved by the streptavidin-peroxidase immunohistochemical method. Antibodies against chromogranin A (CrA), S-100 protein (S-100), P substance (PS), synaptofisin (SYN), neurofilament protein (NF), gliofibrillary acidic protein (GFAP) and neuron specific enolase (NSE) were used. The mean LH and FSH serum concentrations were consistently suppressed with hormonal treatments. Intermediate filaments (NF and GFAP) showed no difference in their expression. The expression of S-100, NSE and SYN was significantly lower in both hormone-treated groups. In oestradiol-treated rats, the immunoreactivity of CrA and SP decreased significantly but was restored after testosterone supplementation. Although the nature and functions of many of these substances in Leydig cells remain unknown, these results are consistent with the hypothesis that the expression of some neuroendocrine markers is hormonally controlled. [source] | ||||||||||