Cyclic AMP regulates somatostatin mRNA accumulation in primary diencephalic cultures and in transfected fibroblast cells

Montminy,; Low, Malcolm J.; Tapia‐Arancibia, Lucía; Reichlin, Seymour; Mandel, Gail; Goodman, RH

doi:10.1523/jneurosci.06-04-01171.1986

Cited by 103 publications

(32 citation statements)

References 17 publications

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“…Total RNA was isolated from untreated cells or from cells treated with forskolin, TSA (100 ng/ml), 15 mM sodium butyrate, or 100 nM trapoxin. Northern blot analysis was performed as described previously, using either an antisense RNA probe to rat somatostatin or an ␣-tubulin cDNA probe (18).…”

mentioning

confidence: 99%

The Phosphorylation Status of a Cyclic AMP-Responsive Activator Is Modulated via a Chromatin-Dependent Mechanism

Michael

Asahara

Shulman

et al. 2000

Molecular and Cellular Biology

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Cyclic AMP (cAMP) stimulates the expression of numerous genes via the protein kinase A (PKA)-mediated phosphorylation of CREB at Ser133. Ser133 phosphorylation, in turn, promotes recruitment of the coactivator CREB binding protein and its paralog p300, histone acetyltransferases (HATs) that have been proposed to mediate target gene activation, in part, by destabilizing promoter bound nucleosomes and thereby allowing assembly of the transcriptional apparatus. Here we show that although histone deacetylase (HDAC) inhibitors potentiate target gene activation via cAMP, they do not stimulate transcription over the early burst phase, during which CREB phosphorylation and CBP/p300 recruitment are maximal. Rather, HDAC inhibitors augment CREB activity during the late attenuation phase by prolonging CREB phosphorylation on chromosomal but, remarkably, not on extrachromosomal templates. In reconstitution studies, assembly of periodic nucleosomal arrays on a cAMP-responsive promoter template potently inhibited CREB phosphorylation by PKA, and acetylation of these template-bound nucleosomes by p300 partially rescued CREB phosphorylation by PKA. Our results suggest a novel regulatory mechanism by which cellular HATs and HDACs modulate the phosphorylation status of nuclear activators in response to cellular signals.

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mentioning

confidence: 99%

The Phosphorylation Status of a Cyclic AMP-Responsive Activator Is Modulated via a Chromatin-Dependent Mechanism

Michael

Asahara

Shulman

et al. 2000

Molecular and Cellular Biology

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“…On the other hand, we previously showed that cAMP increased SRIH biosynthesis in experiments conducted with rat hypothalamic neurons or in NIH-3T3 fibroblast cells transfected with the rat SRIH gene (Montminy et al 1986). Within the SRIH gene, a cAMP-responsive element has also been detected (Montminy et al 1986).…”

Section: Figurementioning

confidence: 95%

“…Within the SRIH gene, a cAMP-responsive element has also been detected (Montminy et al 1986). CREB is probably one signaling pathway by which BDNF activates SRIH gene expression in hypothalamic neurons.…”

Section: Figurementioning

confidence: 99%

Involvement of brain-derived neurotrophic factor in the regulation of hypothalamic somatostatin in vivo

Givalois¹,

Naert²,

Tapia‐Arancibia³

et al. 2006

Journal of Endocrinology

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Brain-derived neurotrophic factor (BDNF) has been extensively studied in the central nervous system as a survival and differentiation factor and in plasticity processes. In vitro, BDNF has been shown to stimulate cellular differentiation and neurohormones synthesis and release. We demonstrated that BDNF is a potent and specific stimulatory agent of somatostatin (SRIH) synthesis in primary cultures of hypothalamic neurons. However, less information is available about its function on SRIH neurons in vivo. In the present study, we examined the effect of in vivo intracerebroventricular BDNF administration in adult non-anesthetized male rats. Two distinct experimental approaches were used: acute intracerebroventricular injection and long-term (14 days) continuous infusion (Alzet micro-pumps). We demonstrate that single intracerebroventricular BDNF injections (5 µg/rat) induce an early (60 and 180 min) decrease in the SRIH mRNA signal in the hypothalamic periventricular nucleus (PeVN) accompanied by a decrease of the hypothalamic SRIH content. 48 h after the acute injection, SRIH mRNA levels and peptide content strongly and significantly increased. After continuous intracerebroventricular BDNF administration (12 µg/day for 14 days), a significant increase in the SRIH hypothalamic content was observed. Nevertheless, the increase in peptide content was not correlated with a similar increase in the PeVN messenger level. These findings show the involvement of BDNF in the in vivo regulation of somatostatinergic neurons in adult rats, which clearly differs according to the BDNF administration mode.

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“…In addition, tissue-specific promoter elements consisting of TAAT motifs that operate in concert with CRE to provide high-level constitutive activity are reiterated three times over a 500-nucleotide region (150). Many of the agents that influence SST secretion are also capable of altering SST gene expression ( (1,131,153,205). cAMP is a potent activator of both gene transcription and secretion of SST and has emerged as the most prominent signaling pathway for regulating SST function.…”

Section: Regulation Of Somatostatin Secretion and Gene Expressionmentioning

confidence: 99%

Biology of Somatostatin and Somatostatin Receptors in Breast Cancer

Patel¹

2000

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate tor Information Operations and Reports, 1215 Jefferson D&vis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Proiect (0704-0188), Washington, DC 20503. AGENCY USE ONLY (Leave blank)REPORT DATE September 1999 REPORT TYPE AND DATES COVEREDAnnual (12 Aug 98 -11 Aug 99) TITLE AND SUBTITLE Biology of Somatostatin and Somatostatin Receptors in Breast Cancer AUTHOR(S)Yogesh C. Patel, M.D., Ph.D. FUNDING NUMBERSDAMD17-96-1-6189 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)McGill UniversityMontreal, Quebec, Canada H3A1A1 ABSTRACT (Maximum 200Analysis of SSTR1-5 mRNA expression by semiquantitative RT-PCR in two separate batches of primary ductal NOS breast cancer (n, N 48 and 50) has revealed a strong positive correlation (p , 0.001) between SSTR3 expression and tumor grade suggesting that SSTR3 induction in high grade tumors may represent a compensatory mechanism for regulating proliferative activity through apoptosis. Expression of SSTR1, 2, and 4 strongly correlates with estrogen receptor levels and SSTR2 expression additionally correlates positively with progesterone receptor levels. Tamoxifen exhibits a dose-dependent biphasic effect on SSTR1 and SSTR5 mRNA, low doses being inhibitory and high doses being stimulatory. SST induces apoptosis selectively through the SSTR3 subtype. This effect is dependent on activation of SHP-1 and caspase-8-mediated decrease in intracellular pH. SST induced apoptosis is not dependent on disruption of mitochondrial function and caspase-9 activation and is inhibited by cAMP-mediated prevention of acidification. Acting via subtypes 1, 2,4, 5, SST exerts cytostatic action by SHPmediated induction of the hypophosphorylated form of the retinoblastoma protein Rb and p21. These signalling events are dependent on regulatory domains in the receptor C-tail. Antisense knockout of endogenous SSTRs in MCF-7 cells has demonstrated a relatively higher potency of SSTR3 and SSTR5 compared to SSTR1 and SSTR2 for inducing antiproliferation.

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Cyclic AMP regulates somatostatin mRNA accumulation in primary diencephalic cultures and in transfected fibroblast cells

Cited by 103 publications

References 17 publications

The Phosphorylation Status of a Cyclic AMP-Responsive Activator Is Modulated via a Chromatin-Dependent Mechanism

The Phosphorylation Status of a Cyclic AMP-Responsive Activator Is Modulated via a Chromatin-Dependent Mechanism

Involvement of brain-derived neurotrophic factor in the regulation of hypothalamic somatostatin in vivo

Biology of Somatostatin and Somatostatin Receptors in Breast Cancer

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