Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An understanding of the functional significance of the newly identified estrogen receptor (ER beta) in the brain will require definition of its expression pattern and relationship to ER alpha. Using an antibody generated against the C-terminus of rat ER beta, we report the presence of ER beta immunoreactivity in the lateral septum, medial amygdala, hippocampus and paraventricular nucleus (PVN) of ovariectomized rats. Double labelling studies in the PVN revealed that approximately 35% of oxytocin neurons located principally in the medial and lateral parvocellular divisions of the caudal PVN were immunoreactive for ER beta while vasopressin, somatostatin and magnocellular oxytocin neurons exhibited no ER beta staining with this antibody. No ER alpha immunoreactive cells were identified in the caudal PVN. These observations provide direct evidence for the differential expression of ER sub-types within neurons and indicate that ER beta may be of physiological significance in the regulation of hypothalamic parvocellular oxytocin neurons by estrogen.
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PMID:Differential expression of estrogen receptor alpha and beta immunoreactivity by oxytocin neurons of rat paraventricular nucleus. 941 30

Growth hormone (GH) synthesis and release from pituitary somatotropes is controlled by the opposing actions of the hypothalamic neuropeptides, GH-releasing hormone (GHRH) in the arcuate nucleus (ARC), and somatostatin in the periventricular nucleus (PeV) and ARC. There is a striking sex difference in the pattern of GH secretion in rats. We have previously demonstrated in male rats that 70% of GHRH neurons in the ARC contain the estrogen receptor alpha (ER alpha) gene, whereas less than 5% of somatostatin neurons in the ARC and PeV expressed the ER alpha or ER beta gene. In addition, it has been reported that the PeV somatostatin neurons of neither sex possess ER immunoreactivity. However, there is no available data about colocalization of ERs and GHRH and/or somatostatin in the ARC of female rats. In this study, we used in situ hybridization in the adult female rat brain to determine whether GHRH neurons and/or somatostatin neurons in the ARC coexpress the ER alpha or ER beta gene. In the ARC, ER alpha mRNA was seen in the ventrolateral region where GHRH mRNA signals were also observed, and in the dorsomedial region where somatostatin mRNA signals were also observed. From studies using adjacent sections through these areas, the distribution of these cells appeared to overlap in part with that of cells containing ER alpha mRNA. On the other hand, few positive cells for ER beta mRNA were observed in the ARC. The double-label in situ hybridization studies showed that in the ARC, 73.4% of GHRH neurons contain ER alpha mRNA, whereas less than 5% of somatostatin neurons express the ER alpha gene. These results indicated that the majority of the GHRH neurons in ARC have ER alpha, but not ER beta, and few somatostatin neurons in ARC have ER alpha or ER beta in either adult female or male rats, suggesting that colocalization with ERs in GHRH and/or somatostatin neurons is not an important determinant of the gender specific pattern of GH secretion.
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PMID:The estrogen receptor (ER) alpha, but not ER beta, gene is expressed in hypothalamic growth hormone-releasing hormone neurons of the adult female rat. 1581 59

This study was designed to investigate the effect of somatostatin on oocytes maturation and subsequent embryo development in cattle. Bovine granulosa cells separated from oocytes, cultured for 24 h and transfected with pEGFP-N1 vector with mouse SST gene (Experimental) and with out plasmid transfection (Control). RT-PCR and Real-Time PCR were used to estimate the expression of bovine receptors of androgen, estrogen beta, growth hormone, and follicular stimulating hormone. Culture media concentrations of hormones were measured by kits using radioimmunoassay. COCs aspirated from ovaries were co-cultured with granulosa cells layers (transfected or control) at 38.5 degrees C in CO(2) incubator for maturation. We found a significant (2.37X) increase in estrogen receptor beta expression in experimental group. There was a decrease in androgen receptor, growth hormone releasing hormone receptor, and follicular stimulating hormone receptor (P < 0.05). But, 96 h of post transfection, culture media concentration of estradiol-17beta was increased significantly (P < 0.05) and testosterone, growth hormone and follicular stimulating hormone showed opposite trend (P < 0.05) in experimental groups. Co-culture of somatostatin transfected granulosa cells with oocytes, reduced the maturation rate from 70% to 66% but had no effect on subsequent fertilization and embryo development.
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PMID:Somatostatin can alter fertility genes expression, oocytes maturation, and embryo development in cattle. 1954 10

The role of the newly discovered estrogen receptor GPR30 in islet physiology and pathophysiology is unclear. We examined GPR30 expression in relation to hormone secretion and possible anti-apoptotic effects in isolated mouse islets using the synthetic GPR30 ligand G-1. The mRNA and protein expression of GPR30 was analyzed by qPCR, Western blot and confocal microscopy. Hormone secretion and cAMP content were determined with RIA and apoptosis in islet cells with the Annexin-V method. GPR30 mRNA and protein expression was markedly higher in islets from females compared to male. This gender difference was not found for the genomic estrogen receptors ER alpha and ER beta, the ER alpha expression being 10-fold higher than ER beta in both genders. Confocal microscopy revealed abounden GPR30 expression in insulin, glucagon and somatostatin cells. Dose-response studies of G-1 vs 17beta-estradiol in isolated islets at 1 or 12 mM glucose showed an almost identical pattern in that both compounds increased insulin and inhibited glucagon and somatostatin secretion. ICI-182,780 and EM-652, potent antagonists of the 17beta-estradiol receptors (ER alpha and ER beta) did not influence the amplifying effect of G-1 or 17beta-estradiol on cAMP content or insulin secretion from isolated islets. Cytokine-induced (IL-1 beta+TNFalpha+INF gamma) apoptosis in islets, cultured for 24h at 5mM glucose, was almost abolished by G-1 or 17beta-estradiol treatment. Addition of ICI-182,780 or EM-652 did not affect this beneficial effect of G-1 or 17beta-estradiol. Taken together, our findings show that GPR30 is expressed in most islet endocrine cells. The synthetic GPR30 ligand G-1 mimics the non-genomic effects of 17beta-estradiol on islet hormone secretion, cAMP content in islets and its anti-apoptotic effects. G-1 or analogs thereof might be new potential candidates in the therapeutic strategy for type 2 diabetes in women.
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PMID:Activation of G protein-coupled receptor 30 modulates hormone secretion and counteracts cytokine-induced apoptosis in pancreatic islets of female mice. 2012 88