Amplification of calcium-induced gene transcription by nitric oxide in neuronal cells

Peunova, Natalia; Enikolopov, Grigori

doi:10.1038/364450a0

Cited by 287 publications

(150 citation statements)

References 27 publications

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“…Alternative roles for NO in immunemediated inflammation could be regulation of blood flow in the reparative phase of inflammation (Moncada et al, 1991;Pons et al, 1993), or reduction of leukocyte adherence and emigration after the initial injury (Arndt et al, 1993). Another function for NO not apparently related to inflammatory damage could be the recently reported synergistic effect with calcium in gene transcription linked to an increase in binding activity of the AP-1 transcription factor comprising the Fos and Jun family proteins (Peunova & Enikolov, 1993).…”

Section: Discussionmentioning

confidence: 99%

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Steil¹,

Garcia‐Rodriguez²,

Crespo³

1995

British J Pharmacology

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1 The involvement of platelet-activating factor (PAF) in immune complex-induced/polymorphonuclearmediated tissue injury was studied by use of a reverse passive Arthus (RPA) model in the peritoneal cavity of rats. 2 Extravasation of protein-rich plasma, accumulation of polymorphonuclear leukocytes (PMN), and the production of nitric oxide (NO) by resident peritoneal mononuclear phagocytes were assayed. 3 Treatment of rats with either UR-12460 or BB-823, two compounds which possess different chemical structures, but elicit the same antagonistic effect on the PAF receptor, abrogated protein-rich plasma extravasation. In contrast, they did not show any effect on the accumulation of PMN. 4 Inhibition of NO production with both N1-mono methyl-L-arginine and N0-nitro-L-arginine failed to prevent protein-rich plasma extravasation. 5 The production of NO by peritoneal adherent cells following RPA was measured in cells maintained for 2 to 28 h in culture, and it was significantly increased in cells removed as early as 15 min after RPA induction, as compared to controls. 6 Addition of 10 nM PAF to the culture medium reduced the generation of NO by peritoneal cells from RPA rats, whereas this mediator enhanced NO production in cells from naive control animals. 7 Treatment with either UR-12460 or BB-823 prior to the induction of RPA produced an almost complete inhibition of NO production. 8 Assay of nitric oxide synthase activity in cell homogenates from peritoneal cells showed that the activity was due to the inducible form of the enzyme. 9 Study by Northen blotting of mRNA coding for the inducible NO synthase (iNOS) showed transcription at 6 and 18 h after the induction of RPA, which was inhibited in UR-12460-treated rats. 10 These data indicate that PAF is the main mediator of the early plasma leakage observed in RPA, and also that PAF is implicated in the triggering of long-term changes via induction of specific genes, as judged from its ability to promote the expression of iNOS.

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Section: Discussionmentioning

confidence: 99%

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Steil¹,

Garcia‐Rodriguez²,

Crespo³

1995

British J Pharmacology

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“…These findings suggest that CREB, CREM and ATF-I are common targets that integrate signals conveyed by the activation of two different transduction pathways, one CAMP-dependent and the other Ca"/calmodulindependent. Interestingly, it has recently been reported that nitric oxide amplifies Ca2 + -induced gene transcription in neuronal cells through a mechanism that may involve CREB phosphorylation by PKA (63). Therefore, both pathways may interact at different levels of the signal transduction cascade.…”

Section: Convergence Of Different Signal Transduction Pathways On Crementioning

confidence: 99%

Transcriptional Control of Gene Expression by cAMP‐Response Element Binding Proteins

Vallejo

1994

J Neuroendocrinology

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“…In this view our present findings would suggest that EDNO is an activator of renin secretion and of renin gene expression in vitro and in vivo, which appears to be involved importantly in the control of renin gene expression by the renal perfusion pressure. A direct stimulatory effect of EDNO on transcriptional activity was in fact recently demonstrated for PC12 cells [19]. To examine the mechanisms along which EDNO could activate renin gene expression on the level of JG cells will be a task for our future work.…”

Section: Discussionmentioning

confidence: 99%

Endothelium derived relaxing factor is involved in the pressure control of renin gene expression in the kidney

et al. 1994

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Abstract.To study the influence of endothelium derived relaxing factor/nitric oxide (EDNO) on renin gene expression, the effects of a 2-day treatment with the NOsynthase inhibitor nitro-L-arginine-methylester (L-NAME, 40 mg/kg twice a day) on plasma renin activity (PRA) and renal and adrenal renin m-RNA levels were examined in conscious rats with and without unilateral renal clips (0.2 ram). In sham-clipped animals L-NAME led to a decrease of PRA from 7.5 to 2.5 ng angiotensin I (ANGI) 9 h -1 9 m1-1 and to a 35% decrease of renal renin m-RNA levels. Unilateral renal artery clipping increased PRA to 35 and to 13 ng ANGI. h -1 9 m1-1 in vehicle and in L-NAME-treated rats, respectively. In the clipped kidneys renin m-RNA levels increased to 450% of control values in vehicle-treated animals and to 220% of control values in L-NAME-treated animals. In the contralaterals as opposed to clipped kidneys, renin m-RNA levels decreased to 16% and 50% of the control values in vehicle-and in L-NAME-treated animals, respectively. In the adrenal glands renin m-RNA levels were not significantly changed either by clipping of one renal artery or by treatment of animals with L-NAME. The NO-donor sodium nitroprusside (100 ~tM) was found to increase renin secretion and renin m-RNA levels in primary cultures of renal juxtaglomerular cells. These findings suggest that EDNO is involved in the control of the renin gene by the renal perfusion pressure.

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Amplification of calcium-induced gene transcription by nitric oxide in neuronal cells

Cited by 287 publications

References 27 publications

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Transcriptional Control of Gene Expression by cAMP‐Response Element Binding Proteins

Endothelium derived relaxing factor is involved in the pressure control of renin gene expression in the kidney

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