ArticleMolecular endocrinology (Baltimore, Md.)2014
Constitutive somatostatin receptor subtype-3 signaling suppresses growth hormone synthesis.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Trial
- Selective ligand recognition and activation of somatostatin receptors SSTR1 and SSTR3.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Agonists, Antagonists and Receptors of Somatostatin: Pathophysiological and Therapeutical Implications in Neoplasias.Current issues in molecular biology · 2024Review
- Article
- Somatostatin-SSTR3-GSK3 modulates human T-cell responses by inhibiting OXPHOS.Frontiers in immunology · 2024Article
- Influence of Leptin on the Secretion of Growth Hormone in Ewes under Different Photoperiodic Conditions.International journal of molecular sciences · 2023Article
- Regulatory Mechanisms of Somatostatin Expression.International journal of molecular sciences · 2020Review
- Somatostatin receptor subtype 5 modifies hypothalamic-pituitary-adrenal axis stress function.JCI insight · 2018Article
- International Union of Basic and Clinical Pharmacology. CV. Somatostatin Receptors: Structure, Function, Ligands, and New Nomenclature.Pharmacological reviews · 2018Review
- Review
- Identification of Phosphorylation Sites Regulating sst3 Somatostatin Receptor Trafficking.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Protective effects of monosialotetrahexosylganglioside sodium on HExperimental and therapeutic medicine · 2015Article
- X-linked acrogigantism syndrome: clinical profile and therapeutic responses.Endocrine-related cancer · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Somatostatin signals through somatostatin receptor subtypes (SSTR) 2 and 5 to attenuate GH secretion. Although expressed in normal pituitary glands and in GH-secreting pituitary tumors, SSTR3 function was unclear, and we have now determined the role of SSTR3 in somatotroph function. Stable rat pituitary tumor cell (GC) transfectants of human SSTR3 (GpSSTR3(WT)) showed suppression of rat (r) GH promoter activity, GH mRNA expression, and secreted GH concordant with suppressed cAMP/protein kinase A (PKA) signaling. In contrast, cAMP levels and GH expression were unchanged in cells expressing a mutant SSTR3 DRY motif (GpSSTR3(R141A)). GH expression was rescued by treatment of GpSSTR3(WT) with forskolin and 8-bromo-cAMP. GpSSTR3(WT) exhibited activation of glycogen synthase kinase3-β (GSK3-β), a PKA substrate, which was also reversed by 8-Bromo-cAMP treatment. Moreover, SSTR3-dependent GH transcriptional inhibition was rescued by inhibition of GSK3-β. GpSSTR3(WT) exhibited elevated Pit-1 serine phosphorylation and decreased Pit-1 occupancy of the rGH promoter with sustained Pit-1 expression. GSK3-β and Pit-1 physically interacted with each other, indicating that Pit-1 may be a GSK3-β phosphorylation substrate. In conclusion, constitutive SSTR3 activity mediates transcriptional repression of GH through cAMP/PKA, leading to subsequent activation of GSK3-β and increased Pit-1 phosphorylation and ultimately attenuating Pit-1 binding to the rGH promoter.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.