Vasopressin gene expression is stimulated by cyclic AMP in homologous and heterologous expression systems

Verbeeck, Marleen A.E.; Adan, Roger A.H.; Burbach, J. Peter H.

doi:10.1016/0014-5793(90)80455-r

Cited by 42 publications

(18 citation statements)

References 26 publications

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“…This is likely to be an important pathway for TRH regulation in all species given that Site 4 is conserved in the TRH promoter of all species studied to date. Furthermore, CREB is an important transcriptional regulator of other PVHexpressed genes including corticotropin-releasing hormone (CRH) and vasopressin (29)(30)(31).…”

Section: Resultsmentioning

confidence: 99%

Transcriptional regulation of the thyrotropin-releasing hormone gene by leptin and melanocortin signaling

Harris¹,

Aschkenasi²,

Elias³

et al. 2001

J. Clin. Invest.

310

221

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IntroductionThe hypothalamic peptide, thyrotropin-releasing hormone (TRH), is essential for the normal production of thyroid-stimulating hormone in the pituitary and thyroid hormones in the thyroid gland (1). Within the paraventricular hypothalamic nucleus (PVH), TRH is regulated at the transcriptional level by thyroid hormone (T3), such that in hyperthyroid states TRH expression is reduced and in hypothyroid states its expression is increased (2). Recently, it has become clear that TRH is also regulated by nutritional states. To conserve energy during periods of food deprivation, rodents dramatically reduce their thyroid hormone levels, which in turn allows reductions in their metabolic rate (3). This adaptation to starvation is accomplished through a reduction in the expression of TRH in the PVH, indicating that a central process contributes to the regulation of this physiological adaptation. The mechanism governing the nutritional regulation of TRH has been clarified by Ahima et al., who reversed starvation-induced suppression of thyroid hormone levels in mice by administering leptin during starvation (4). This finding was extended by Legradi et al., who further demonstrated that leptin's effects were due to upregulation of TRH gene expression (5).Although leptin can regulate TRH gene expression in the PVH, it remains unclear whether this effect is mediated by direct actions of leptin on the TRH neuron in the PVH or indirectly through leptin effects on other neurons, which then project to the TRH neuron.Recently Legradi et al. demonstrated that chemical ablation of the arcuate nucleus blocks leptin's effect on TRH expression, suggesting that an indirect pathway is involved (6). Given that leptin activates pro-opiomelanocortin (POMC) gene expression in the arcuate nucleus, POMC-derived α-melanocyte stimulating hormone (α-MSH) is a candidate hormone that may be responsible for the regulation of TRH expression (7,8). Starvation causes a rapid reduction in thyroid hormone levels in rodents. This adaptive response is caused by a reduction in thyrotropin-releasing hormone (TRH) expression that can be reversed by the administration of leptin. Here we examined hypothalamic signaling pathways engaged by leptin to upregulate TRH gene expression. As assessed by leptin-induced expression of suppressor of cytokine signaling-3 (SOCS-3) in fasted rats, TRH neurons in the paraventricular nucleus are activated directly by leptin. To a greater degree, they also contain melanocortin-4 receptors (MC4Rs), implying that leptin can act directly or indirectly by increasing the production of the MC4R ligand, α-melanocyte stimulating hormone (α-MSH), to regulate TRH expression. We further demonstrate that both pathways converge on the TRH promoter. The melanocortin system activates the TRH promoter through the phosphorylation and DNA binding of the cAMP response element binding protein (CREB), and leptin signaling directly regulates the TRH promoter through the phosphorylation of signal transducer and activator of transcription 3 (St...

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Section: Resultsmentioning

confidence: 99%

Transcriptional regulation of the thyrotropin-releasing hormone gene by leptin and melanocortin signaling

Harris¹,

Aschkenasi²,

Elias³

et al. 2001

J. Clin. Invest.

310

221

View full text Add to dashboard Cite

show abstract

“…Nuclear factor-1 inhibits cAMP-induced transcription from the phosphoenolpyruvate carboxykinase gene by binding to block CREB access to CBP (61). The PCR-amplified GR gene promoter elements between Ϫ1523 and Ϫ971 we used in this study include the same nGRE Ϫ1485 -cAMP Ϫ1461 regulatory motifs separated by 25 bp but exclude the putative nuclear factor-1 Ϫ1530 recognition motif.…”

Section: Discussionmentioning

confidence: 99%

Recruitment of cAMP-response Element-binding Protein and Histone Deacetylase Has Opposite Effects on Glucocorticoid Receptor Gene Transcription

Govindan

2010

Journal of Biological Chemistry

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Glucocorticoids control the synthesis of the glucocorticoid receptor (GR) in various tissues through a negative feedback regulation of the mRNA. In this study, we have identified feedback regulatory domains in the human GR gene promoter and examined the roles of GR, the cAMP-response element-binding protein (CREB), and HDAC-6 in association with promoter elements of the human GR gene. Using breast cancer T47D and HeLa-GR cells, we identify specific negative glucocorticoid-response elements in the GR gene. The feedback regulatory domains were also involved in interactions with CREB. GR-bound negative glucocorticoid-response elements recruited HDAC-6, and this was dependent on treatment with dexamethasone. Both CREB and HDAC-6 formed complexes with GRdexamethasone. The HDAC-6 LXXLL motif between amino acids 313 and 418 made direct contact with the GR AF-1 domain. Interestingly enough, although the level of GR decreased in CREB knockdown cells, it was elevated in HDAC-6 knockdown cells. Our results suggest that CREB-P is dephosphorylated and that HDAC-6 is recruited by the GR, and they play opposite roles in the negative feedback regulation of the GR gene.

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“…The nature of the VP gene products needs to be investigated. The VP-expressing SCLC cell line GLC-8 has provided a valuable model for studies on VP gene regulation in neo plastic tissue [45,46].…”

Section: Discussionmentioning

confidence: 99%

Expression of the Vasopressin and Gastrin-Releasing Peptide Genes in Small Cell Lung Carcinoma Cell Lines

et al. 1992

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Various polypeptide hormones including vasopressin (VP) and gastrin-releasing peptide (GRP) are produced by small cell lung carcinomas (SCLC). VP as well as GRP have mitogenic effects on several cell types and are proposed to be autocrine growth factors. In this study the presence of VP mRNA, oxytocin (OT) mRNA and GRP mRNA was investigated in cell lines derived from SCLCs. Out of 26 cell lines 3 contained low amounts of VP mRNA (GLC-8, SCLC-21H and NCI-H345) and 7 contained abundant GRP mRNA (GLC-16, GLC-1-M13, SCLC-22H, NCI-H249, NCI-H345, NCI-H449 and NCI-H450). The GRP mRNA-containing cell lines belong to the classic SCLC type, whereas VP mRNA was found in two classic and one variant cell line. None of the SCLC cell lines contained detectable levels of OT mRNA. Of the three VP-expressing SCLC cell lines, GLC-8 had the highest level of VP mRNA. Both the length of the transcript and the hybridization with different probes containing exons A and C of the VP gene suggest that the detected transcript is a normal VP messenger. SCLC GLC-8 contained low levels of VP immunoreactivity and VP receptors. In GLC-8 an autocrine role of VP may be suspected.

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Vasopressin gene expression is stimulated by cyclic AMP in homologous and heterologous expression systems

Cited by 42 publications

References 26 publications

Transcriptional regulation of the thyrotropin-releasing hormone gene by leptin and melanocortin signaling

Transcriptional regulation of the thyrotropin-releasing hormone gene by leptin and melanocortin signaling

Recruitment of cAMP-response Element-binding Protein and Histone Deacetylase Has Opposite Effects on Glucocorticoid Receptor Gene Transcription

Expression of the Vasopressin and Gastrin-Releasing Peptide Genes in Small Cell Lung Carcinoma Cell Lines

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