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Ovarian Kaleidoscope Database (OKdb)

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somatostatin receptor 2 OKDB#: 2213
 Symbols: SSTR2 Species: human
 Synonyms:  Locus: 17q25.1 in Homo sapiens
HPMR


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General Comment NCBI Summary: Somatostatin acts at many sites to inhibit the release of many hormones and other secretory proteins. The biologic effects of somatostatin are probably mediated by a family of G protein-coupled receptors that are expressed in a tissue-specific manner. SSTR2 is a member of the superfamily of receptors having seven transmembrane segments and is expressed in highest levels in cerebrum and kidney. [provided by RefSeq, Jul 2008]
General function Receptor
Comment
Cellular localization Plasma membrane
Comment
Ovarian function Initiation of primordial follicle growth, Follicle atresia, Steroid metabolism
Comment Treatment of female rhesus macaques with a somatostatin receptor antagonist that increases oocyte fertilization rates without affecting post-fertilization development outcomes. Ting AY et al. (2018) To determine the effects of PGL1001, a somatostatin receptor isoform-2 (SSTR-2) antagonist, on ovarian follicle development, oocyte fertilization, and subsequent embryo developmental potential in the rhesus macaque. Cycling female rhesus macaques (N = 8) received vehicle through one menstrual (control) cycle, followed by daily injections of PGL1001, a SSTR-2 antagonist, for three menstrual (treatment) cycles. Main endpoints include overall animal health and ovarian hormones (e.g., estradiol E2], progesterone [P4], and anti-Müllerian hormone [AMH]), ovarian circumference, numbers of oocytes and their maturation status following controlled ovarian stimulation (COS), as well as oocyte fertilization and subsequent blastocyst rates that were assessed in control and PGL1001 treatment cycles. Circulating PGL1001 levels were assessed at baseline as well as 6, 60, and 90 days during treatment. PGL1001 treatment did not impact overall animal health, menstrual cycle length, or circulating levels of ovarian hormones (E2, P4, and AMH) in comparison to vehicle treatment during natural cycles. PGL1001 treatment increased (p ˂ 0.05) ovarian circumference and the day 8 to day 1 ratio of AMH levels (p ˂ 0.05) during a COS protocol, as well as oocyte fertilization rates compared to the vehicle treatment interval. Blastocyst development rates were not significantly different between vehicle and PGL1001 treatment groups. Prolonged treatment with PGL1001 appears to be safe and does not affect rhesus macaque general health, menstrual cycle length, or ovarian hormone production. Interestingly, PGL1001 treatment increased the fertilization rate of rhesus macaque oocytes collected following ovarian stimulation.////////////////// Kit Ligand and the Somatostatin Receptor Antagonist, BIM-23627, Stimulate in Vitro Resting Follicle Growth in the Neonatal Mouse Ovary. [Gougeon A et al. In the mammalian ovary, kit ligand (KL), coded by a cAMP-stimulatable gene, is a protein that promotes initiation of follicle growth. The neuropeptide somatostatin (SST) is a small peptide that inhibits cAMP generation in many cell types. Consequently, SST receptor agonists might alter KL production and subsequent follicle growth. The present study was undertaken to look for the existence of a functional SST system in the mouse ovary, to test the effects of the SST receptor 2 (SSTR-2) antagonist BIM-23627 on in vitro folliculogenesis, and to compare them with those of KL, which was demonstrated to stimulate follicle growth in the neonatal rat ovary. Pairs of ovaries from 5-d-old mice were incubated in vitro during 15 d in the presence of either KL or BIM-23627. For every mouse, one ovary was cultured in culture medium (control), and the other ovary was cultured in the presence of either KL or BIM-23627. After 5, 10, and 15 d culture, the ovaries were histologically assessed for the content of primordial, primary, and secondary follicles. The SSTR-2 and -5, but not SST, were identified at the transcriptional and translational (mainly in granulosa cells) levels. Both KL and BIM-23627 triggered a reduction of the percentages of primordial follicles and an increase of the percentages of primary and secondary follicles when compared with control ovaries from the same animal. In conclusion, extraovarian SST, acting through its receptors 2 and 5 present on granulosa cells, may be involved in mouse folliculogenesis by reducing recruitment of resting follicles.
Expression regulated by FSH
Comment Constitutive and follicle-stimulating hormone-induced action of somatostatin receptor-2 on regulation of apoptosis and steroidogenesis in bovine granulosa cells. Riaz H 2014 et al. In the present study, we employed primary bovine culture of granulosa cells (GCs) as a cellular model to study the potential involvement of somatostatin receptor 2 (SSTR2) in ovarian function. The results showed that bovine GCs expressed SST2 receptor and further found that SSTR2 was possibly regulated by follicle-stimulating hormone (FSH), as a significant increase in protein level of SSTR2 was observed in FSH-treated GCs. For further analysis, endogenous SSTR2 expression was disrupted using small inhibitory RNA (siRNA) and the efficacy of differential silencing of endogenous SSTR2 expression was measured both at transcriptional and translational levels. Transient blockage of SSTR2 evidenced its constitutive action on GCs, as it significantly increased level of cAMP (2.4-folds) and basal progesterone production (~2-fold, P<0.05) with significant increase (P<0.05) in mRNA levels of StAR and P450ssc without altering estradiol concentration and aromatase mRNA expression. Furthermore, silencing of SSTR2 reduced GCs apoptosis (52.5%, P<0.05) and increased cell proliferation, which was further corroborated by up-regulation in protein expressions of B-cell leukemia/lymphoma 2 (Bcl-2), inhibition of caspase3 and mRNA level of bcl2-associated-X protein (Bax). These results provide evidence that SSTR2 subtype controls GCs apoptosis, proliferation and hormonal secretions through selective constitutive action, independently of somatostatin (SST). Given the local inhibitory actions of SSTR2 on the gonads, we further found that apoptosis in ssRNAi-2 transfected cells decreased (6.8% Vs 1.9%, P<0.05) more strongly on FSH treatment. Apoptotic protein expressions and steroid hormone mRNA levels were correlated with a relative decrease in apoptosis and increase in progesterone production. Our results suggest that SSTR2 may play a crucial role as local inhibitor of FSH action on GCs apoptosis and steroidogenesis. /////////////////////////
Ovarian localization Granulosa, Tumor cell
Comment This gene was found in a mouse DNA array analysis of transcripts expressed in mouse preovulatory follicles. Reubi JC, et al. (Cancer Res. 1994) evaluatd somatostatin receptor gene expression of SSTR1, SSTR2, and SSTR3 subtypes by in situ hybridization in 55 human primary tumors shown to contain a high density of somatostatin receptors in binding assays. They found that All 55 tumors expressed at least one SSTR subtype. Of 55 somatostatin receptor-positive tumors, 46 had SSTR2 mRNA; all 46 were characterized as having receptors with a high affinity for the synthetic analogue octreotide. Of 55 tumors, 12 expressed SSTR1, and 14 expressed SSTR3 mRNA. The subtype SSTR1 was expressed alone in 4 cases, SSTR2 was expressed alone in 33 cases, and SSTR3 was expressed alone in one case. In 4 cases, all 3 SSTR were expressed simultaneously. The cases having SSTR1 mRNA were identified in binding experiments with 125I-labeled somatostatin-14 and -28 analogues rather than with 125I-[Tyr3]-octreotide. Whereas meningiomas, neuroblastomas, pituitary adenomas, small cell lung carcinomas, lymphomas, and breast tumors expressed primarily a high abundance of SSTR2, carcinoids, islet cell carcinomas, medullary thyroid carcinomas, and ovarian tumors had a mixed distribution of the somatostatin receptor subtypes.
Follicle stages
Comment
Phenotypes
Mutations 0 mutations
Genomic Region show genomic region
Phenotypes and GWAS show phenotypes and GWAS
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created: Oct. 14, 2003, 12:33 p.m. by: xin   email:
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last update: Nov. 28, 2018, 2:20 p.m. by: hsueh    email:



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