Orthovanadate Stimulates cAMP Phosphodiesterase 3 Activity in Isolated Rat Hepatocytes through Mitogen-Activated Protein Kinase Activation Dependent on cAMP-Dependent Protein Kinase

Watanabe, Tomoyasu; Satoo, Hirofumi; Kohara, Kazuhisa; Takami, Reiko; Motoyashiki, Toshio; Morita, Tetsuo; Ueki, Hiroshi

doi:10.1248/bpb.27.789

Cited by 11 publications

(13 citation statements)

References 73 publications

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“…Our previous study, however, demonstrated that during a hepatic warm ischemia-reperfusion systemic hemodynamics were not affected by a milrinone pretreatment, while the milrinone pretreatment significantly ameliorated postischemic hepatic microcirculation. PDE3 is naturally distributed in liver tissue, platelets, adipose tissue and immunocytes, as well as the cardiovascular system [3][4][5]. The function of PDE3 may be important for local circulatory, metabolic and inflammatory reactions during a warm ischemia-reperfusion insult of the liver [6].…”

Section: Introductionmentioning

confidence: 99%

“…The function of PDE3 may be important for local circulatory, metabolic and inflammatory reactions during a warm ischemia-reperfusion insult of the liver [6]. In fact, milrinone demonstrates a selective PDE3 inhibitory action in these tissues [3][4][5]. In milrinone-treated rat livers, adenosine 3',5'-cyclic monophosphate (cAMP) concentrations were increased and the acquired ischemic tolerance seemed to be attributable to the increase of cAMP [1].…”

Section: Introductionmentioning

confidence: 99%

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Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Satoh

Kume

Abe

et al. 2009

Journal of Surgical Research

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Satoh

Kume

Abe

et al. 2009

Journal of Surgical Research

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“…Incubation of PC12 and PC12-H 3 cells with BNP (100 nM) significantly decreased the rate of cAMP hydrolysis (an index of PDE3 activity). Insulin (100 nM) (Watanabe et al, 2004) and cilostamide (10 M) (Hidaka et al, 1979), PDE3 activator and inhibitor, respectively, served as controls (Fig. 7, A and B).…”

mentioning

confidence: 99%

Natriuretic Peptide-Induced Catecholamine Release from Cardiac Sympathetic Neurons: Inhibition by Histamine H₃ and H₄ Receptor Activation

Chan

Robador

Levi

2012

J Pharmacol Exp Ther

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We reported previously that natriuretic peptides, including brain natriuretic peptide (BNP), promote norepinephrine release from cardiac sympathetic nerves and dopamine release from differentiated pheochromocytoma PC12 cells. These proexocytotic effects are mediated by an increase in intracellular calcium secondary to cAMP/protein kinase A (PKA) activation caused by a protein kinase G (PKG)-mediated inhibition of phosphodiesterase type 3 (PDE3). The purpose of the present study was to search for novel means to prevent the proadrenergic effects of natriuretic peptides. For this, we focused our attention on neuronal inhibitory G␣ i/o -coupled histamine H 3 and H 4 receptors. Our findings show that activation of neuronal H 3 and H 4 receptors inhibits the release of catecholamines elicited by BNP in cardiac synaptosomes and differentiated PC12 cells. This effect results from a decrease in intracellular Ca 2ϩ due to reduced intracellular cAMP/PKA activity, caused by H 3 and H 4 receptor-mediated PKG inhibition and consequent PDE3-induced increase in cAMP metabolism. Indeed, selective H 3 and H 4 receptor agonists each synergized with a PKG inhibitor and a PDE3 activator in attenuating BNP-induced norepinephrine release from cardiac sympathetic nerve endings. This indicates that PKG inhibition and PDE3 stimulation are pivotal for the H 3 and H 4 receptor-mediated attenuation of BNP-induced catecholamine release. Cardiac sympathetic overstimulation is characteristic of advanced heart failure, which was recently found not to be improved by the administration of recombinant BNP (nesiritide), despite the predicated beneficial effects of natriuretic peptides. Because excessive catecholamine release is likely to offset the desirable effects of natriuretic peptides, our findings suggest novel means to alleviate their adverse effects and improve their therapeutic potential.

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“…V compounds adopt a trigonal bipyramidal structure that mimics the transition state of the phosphoryl transfer reaction, thereby acting either as a competitive inhibitor (VS) or an oxidizer (peroxovanadate complexes) of the conserved cysteine residue in the protein tyrosine phosphatase loop (23). V derivatives can directly activate members of the mitogen-activated protein kinases (24)(25)(26) and induce phosphatidylinositol 3Ј-kinase association to activating docking molecules like insulin receptor substrates (IRSs) (27). In combination with insulin, V compounds can augment͞ prolong insulin receptor and IRS-1 tyrosine phosphorylation (28) and enhance insulin-induced glucose transport (29).…”

mentioning

confidence: 99%

Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness

Johnson

O’Connor

Dantzer

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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To the ill patient with diabetes, the behavioral symptoms of sickness such as fatigue and apathy are debilitating and can prevent recuperation. Here we report that peripherally administered insulin-like growth factor 1 (IGF-1) attenuates LPS-dependent depression of social exploration (sickness) in nondiabetic (db͞ϩ) but not in diabetic (db͞db) mice. We show that the insulin͞IGF-1 mimetic vanadyl sulfate (VS) is effective at augmenting recovery from sickness in both db͞ϩ and db͞db mice. Specifically, peak illness was reached at 2 h for both VS and control animals injected with LPS, and VS mice recovered 50% faster than non-VS-treated animals. Examination of the mechanism of VS action in db͞ϩ mice showed that VS paradoxically augmented peritoneal macrophage responsivity to LPS, increasing both peritoneal and ex vivo macrophage production of IL-1␤ and IL-6 but not TNF-␣. The effects of VS in promoting recovery from sickness were not restricted to LPS, because they were also observed after direct administration of IL-1␤. To explore the possibility that VS impairs immune-to-brain communication via vagal afferents, the vagally mediated satietyinducing effects of cholecystokinin 8 were tested in db͞ϩ mice. Cholecystokinin decreased food intake in saline-injected mice but not in VS-treated mice. VS also inhibited LPS-dependent up-regulation of IL-1␤ and IL-6 mRNA in the brain, while increasing by 50% the cerebral expression of transcripts of the specific antagonist of IL-1 receptors IL-1RA and IL-1R2. Taken together, these data indicate that VS improves recovery from LPS-induced sickness by blocking vagally mediated immune-to-brain signaling and by upregulating brain expression of IL-1␤ antagonists.neuroimmunity ͉ sickness behavior ͉ type 2 diabetes ͉ vanadium S timulation of the peripheral innate immune system by the cytokine inducer LPS causes expression of proinflammatory cytokines in the brain, and this response is associated with development of sickness behavior (1). We have recently shown that type 2 diabetic (db͞db) mice display an enhanced and more prolonged episode of sickness in response to LPS and IL-1␤ (2). How diabetes alters brain-immune interactions however, is still unclear. Insulin resistance is a critical component of type 2 diabetes and is likely responsible for initiation (3). Strategies to maximize insulin sensitivity, increase insulin action, and͞or inhibit insulin counterregulation might be expected to neutralize the deleterious effect of type 2 diabetes on superimposed illness. One agent with antidiabetic properties is vanadium (V). V is a naturally occurring element found in soil and rocks at a concentration of Ϸ150 ppm (4). It does not normally exist in elemental form but is bound most commonly to oxygen, sodium, chloride, and sulfur (5). V has six oxidation states (1Ϫ through 5ϩ), with V ϩ 4 and V ϩ 5 being most common in the body (6). The average human intake of V is 10-20 g͞day, mostly from plant material (5) in the form of sodium metavanadate, sodium orthovanadate, V pentoxide, and vanadyl ...

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Orthovanadate Stimulates cAMP Phosphodiesterase 3 Activity in Isolated Rat Hepatocytes through Mitogen-Activated Protein Kinase Activation Dependent on cAMP-Dependent Protein Kinase

Abstract: These results indicate that vanadate stimulates the particulate PDE3 activity by activating mainly p44 MAPK via a PKA-dependent process, and that it differs from insulin with regard to a phosphorylation cascade of PDE3 activation.

Cited by 11 publications

References 73 publications

Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Natriuretic Peptide-Induced Catecholamine Release from Cardiac Sympathetic Neurons: Inhibition by Histamine H₃ and H₄ Receptor Activation

Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness

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Orthovanadate Stimulates cAMP Phosphodiesterase 3 Activity in Isolated Rat Hepatocytes through Mitogen-Activated Protein Kinase Activation Dependent on cAMP-Dependent Protein Kinase

Abstract: These results indicate that vanadate stimulates the particulate PDE3 activity by activating mainly p44 MAPK via a PKA-dependent process, and that it differs from insulin with regard to a phosphorylation cascade of PDE3 activation.

Cited by 11 publications

References 73 publications

Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Implication of Protein Kinase A for a Hepato-Protective Mechanism of Milrinone Pretreatment

Natriuretic Peptide-Induced Catecholamine Release from Cardiac Sympathetic Neurons: Inhibition by Histamine H3 and H4 Receptor Activation

Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness

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Natriuretic Peptide-Induced Catecholamine Release from Cardiac Sympathetic Neurons: Inhibition by Histamine H₃ and H₄ Receptor Activation