Effects of adenosine analogues on basal, prostaglandin E1- and forskolin-stimulated cyclic AMP formation in intact neuroblastoma cells

Murphy, Mary; Byczko, Zenobia

doi:10.1016/0006-2952(89)90627-8

Cited by 8 publications

(7 citation statements)

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“…We recently demonstrated that N1E-115 neurobIastoma cells contain adenosine receptors that stimulate adenylate cyelase activity, and that the most potent of a series of agonists was the stable adenosine analogue NECA (Murphy and Byczko 1989). In the present study, addition of NECA (10-!-10-~M) to the incubation medium for 20 min resulted in concentration-dependent increases in CAMP formation in both control and linoleate-supplemented cells (Fig.…”

Section: Effects Of P Ufa Enrichment Qn Neca -Stimulated Camp Formationsupporting

confidence: 49%

“…We demonstrated recently that the neuroblastoma cell line N1E-115 contains receptors for adenosine that at high concentrations of agonist stimulate CAMP formation (Murphy and Byczko 1989). The question that followed was whether adenosine receptor function was affected by membrane PUFA environment, since this could be a specific mechanism whereby essential fatty acids could exert a neuroregulatory effect.…”

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Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Murphy

Byczko²

1990

Biochem. Cell Biol.

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We have examined the effects of increasing membrane polyunsaturated fatty acids (PUFAs) on adenosine receptor function in intact N1E-115 neuroblastoma cells. Addition of linoleic acid to the culture medium for 48 h resulted in an approximate threefold increase in the amount of omega 6 fatty acids esterified to membrane phospholipids. Basal cAMP accumulation was significantly higher in the PUFA-enriched cells than in controls, although the differences could be diminished by approximately 75% by treatment of the cells with adenosine deaminase or 8-phenyltheophylline. Exposure of the cultures to the stable adenosine analogue 5'-N-ethylcarboxyamide adenosine (NECA) resulted in concentration-dependent increases in cAMP accumulation. Data from saturation experiments indicated that the maximum amount of cAMP that could be formed in response to NECA in the PUFA-enriched cells was twice that in control cells. Also, the amount of agonist required to elicit half maximal stimulation in the supplemented cells was significantly less than in the control cells (mean values for EC50, 0.85 and 1.43 microM, respectively). The results of this study demonstrate that membrane PUFA have the ability to modify interactions between adenosine receptors and adenylate cyclase in neural cells, a fact that is of potential importance in considering the central role that adenosine plays as a neuromodulator in the nervous system.

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Section: Effects Of P Ufa Enrichment Qn Neca -Stimulated Camp Formationsupporting

confidence: 49%

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confidence: 99%

Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Murphy

Byczko²

1990

Biochem. Cell Biol.

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“…To facilitate the detection of G i/o ‐mediated responses, basal AC activity was enhanced by the addition of 1 μ M forskolin (leading to a robust 725±56% induction of cAMP accumulation, relative to control). At the tested concentration, maximal response to forskolin is certainly not reached, as the EC 50 value of forskolin in mediating cAMP accumulation in N1E‐115 cells is close to 10 μ M ( Stenstrom et al , 1985 ; Murphy and Byczko, 1989 ). In these conditions, both HU210 and CP55940 exhibited a more pronounced inhibition of cAMP formation (50.9 and 56.0% reduction relative to forskolin treated cells, respectively) (Figure 1b).…”

Section: Resultsmentioning

confidence: 95%

Differential modulation of AP‐1‐ and CRE‐driven transcription by cannabinoid agonists emphasizes functional selectivity at the CB₁ receptor

Bosier

Hermans

Lambert

2008

British J Pharmacology

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Background and purpose: Long-term adaptations to pharmacological stimuli frequently originate from modulation of complex intracellular signalling pathways. We previously reported that HU210 and CP55940, two CB 1 cannabinoid receptor agonists, induced opposite effects on TH expression. Herein, we characterized their influence on cAMP response element (CRE) and activator protein 1 (AP-1)-mediated regulation of gene transcription. Experimental approach: The activity of the agonists was examined on transfected N1E-115 cells in which expression of the luciferase reporter gene was controlled by transcription promoters consisting of repeats of either CRE or AP-1 elements. In addition, the implication of classical signalling pathways was investigated using a variety of kinase inhibitors. Key results: Consistent with the CB 1 -mediated reduction of cAMP accumulation, both ligands decreased CRE-driven luciferase expression with similar potencies. HU210 also exhibited a concentration-dependent reduction of luciferase activity in cells engineered to examine AP-1-controlled transcription, whereas such response was not obtained with CP55940. Responses were all inhibited by SR141716A and were modified in Pertussis toxin-treated cells, suggesting agonist-selective regulations of distinct G i/o -dependent mechanisms through CB 1 receptor activation. Finally, PKC inhibitors efficiently inhibited the paradoxical effect of HU210 on AP-1-mediated transcription, indicating selective regulation of PKC-dependent responses. Conclusions and implications:Together, our results demonstrate that two cannabinoid ligands, commonly used as reference agonists acting on the same receptor with similar affinities, differentially modulate gene transcription through distinct controls of AP-1. This could reflect activation of distinct subsets of G i/o -proteins, supporting the concept of functional selectivity at CB 1 receptors.

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“…We next sought to determine whether S 1755 is preferentially phosphorylated at submaximal PKA activation, as was concluded from previous work in vitro [7]. For this study, we examined phosphorylation in response to prostaglandin E 1 (PGE 1 ), which activates adenylyl cylclase through an endogenous G protein‐coupled receptor [23], and produces more moderate increases in cAMP levels than forskolin [24]. Fig.…”

Section: Resultsmentioning

confidence: 99%

The contribution of serine residues 1588 and 1755 to phosphorylation of the type I inositol 1,4,5‐trisphosphate receptor by PKA and PKG

Soulsby

Alzayady

et al. 2003

FEBS Letters

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Type I inositol 1,4,5-trisphosphate receptors can be phosphorylated by cAMP-dependent protein kinase (PKA) and cGMP-dependent protein kinase (PKG). To define the site-specificity of these events we analyzed the phosphorylation of mutant receptors expressed in intact cells. These studies showed that S(1588) and S(1755), the serine residues within kinase consensus sequences, are equally sensitive to PKA, that phosphorylation events at these sites are independent of each other, and that PKG predominantly phosphorylates S(1588). These findings provide the basis for understanding the functional consequences of type I inositol 1,4,5-trisphosphate receptor phosphorylation.

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Effects of adenosine analogues on basal, prostaglandin E1- and forskolin-stimulated cyclic AMP formation in intact neuroblastoma cells

Cited by 8 publications

References 21 publications

Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Differential modulation of AP‐1‐ and CRE‐driven transcription by cannabinoid agonists emphasizes functional selectivity at the CB₁ receptor

The contribution of serine residues 1588 and 1755 to phosphorylation of the type I inositol 1,4,5‐trisphosphate receptor by PKA and PKG

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Effects of adenosine analogues on basal, prostaglandin E1- and forskolin-stimulated cyclic AMP formation in intact neuroblastoma cells

Cited by 8 publications

References 21 publications

Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Effects of membrane polyunsaturated fatty acids on adenosine receptor function in intact N1E-115 neuroblastoma cells

Differential modulation of AP‐1‐ and CRE‐driven transcription by cannabinoid agonists emphasizes functional selectivity at the CB1 receptor

The contribution of serine residues 1588 and 1755 to phosphorylation of the type I inositol 1,4,5‐trisphosphate receptor by PKA and PKG

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Differential modulation of AP‐1‐ and CRE‐driven transcription by cannabinoid agonists emphasizes functional selectivity at the CB₁ receptor