Convergence of Ca2+ signaling pathways in adipocytes. The role of L-arginine and protein kinase G in generation of transient and periodic Ca2+ signals

Turovsky, Egor A.; Turovskaya, M. V.; Berezhnov, Alexey V.; Толмачева, А. В.; Kaimachnikov, Nikolai P.; Долгачева, Л. П.; Зинченко, В. П.; Maevskii, E. I.; Дынник, В. В.

doi:10.1134/s1990747811060158

Cited by 7 publications

(14 citation statements)

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“…4J). These agonists also do not generate sustained oscillations of [Ca 2+ ] i in the absence of ACh in the presented concentration range [14]. Unlike the effect of NE, which induces generations of simple modes of fast Ca 2+ -oscillations in the presence of ACh (Fig.…”

Section: Resultsmentioning

confidence: 66%

“…4A) whereas addition of NE alone in the same concentration range induced either impulse responses in the majority of cells, or fast-damping oscillations in single adipocytes [14]. The addition of low doses of ACh after application of NE also resulted in generation of sustained modes of Ca 2+ oscillations (Fig.…”

Section: Resultsmentioning

confidence: 83%

“…The steady modes of Ca 2+ oscillations observed in adipocytes persist during a short period of time (about 3–4 minutes) in the absence of Ca 2+ in the incubation medium [14] and disappear completely upon depletion of the reticular Ca 2+ pool following incubation of cells with thapsigargin, an inhibitor of the Ca 2+ -ATPase of endoplasmic reticulum (SERCA) (Fig. 2A).…”

Section: Resultsmentioning

confidence: 99%

“…During all the stages of probe loading and washout, as well as during the application of various agonists, the HBSS medium contained 200 µM L-arginine to maintain the active state of eNOS, and cGMP metabolizing enzymes [14]. In the absence of L-arginine basal NO production was detected only in single adipocytes.…”

Section: Methodsmentioning

confidence: 99%

“…Stimulation of parasympathetic nerves results in: acceleration of insulin production by pancreatic β-cells [5]–[7], suppression of glucose production and augmentation of glucose uptake by liver [4]. Acetylcholine (ACh), the principal neurotransmitter of the parasympathetic nervous system, realizes its metabolic effects by activating M 3 -cholinergic receptors (M 3 -AChR) in the pancreas [6]–[8], liver [9], [10], skeletal [11] and smooth [12] muscles and white adipose tissue (WAT) [13], [14]. In pancreatic [15], smooth [12], [16] and skeletal [17] muscle cells M 1,2 AChR may be involved too.…”

Section: Introductionmentioning

confidence: 99%

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Acetylcholine Promotes Ca2+and NO-Oscillations in Adipocytes Implicating Ca2+→NO→cGMP→cADP-ribose→Ca2+ Positive Feedback Loop - Modulatory Effects of Norepinephrine and Atrial Natriuretic Peptide

et al. 2013

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PurposeThis study investigated possible mechanisms of autoregulation of Ca2+ signalling pathways in adipocytes responsible for Ca2+ and NO oscillations and switching phenomena promoted by acetylcholine (ACh), norepinephrine (NE) and atrial natriuretic peptide (ANP).MethodsFluorescent microscopy was used to detect changes in Ca2+ and NO in cultures of rodent white adipocytes. Agonists and inhibitors were applied to characterize the involvement of various enzymes and Ca2+-channels in Ca2+ signalling pathways.ResultsACh activating M3-muscarinic receptors and Gβγ protein dependent phosphatidylinositol 3 kinase induces Ca2+ and NO oscillations in adipocytes. At low concentrations of ACh which are insufficient to induce oscillations, NE or α1, α2-adrenergic agonists act by amplifying the effect of ACh to promote Ca2+ oscillations or switching phenomena. SNAP, 8-Br-cAMP, NAD and ANP may also produce similar set of dynamic regimes. These regimes arise from activation of the ryanodine receptor (RyR) with the implication of a long positive feedback loop (PFL): Ca2+→ NO→cGMP→cADPR→Ca2+, which determines periodic or steady operation of a short PFL based on Ca2+-induced Ca2+ release via RyR by generating cADPR, a coagonist of Ca2+ at the RyR. Interplay between these two loops may be responsible for the observed effects. Several other PFLs, based on activation of endothelial nitric oxide synthase or of protein kinase B by Ca2+-dependent kinases, may reinforce functioning of main PFL and enhance reliability. All observed regimes are independent of operation of the phospholipase C/Ca2+-signalling axis, which may be switched off due to negative feedback arising from phosphorylation of the inositol-3-phosphate receptor by protein kinase G.ConclusionsThis study presents a kinetic model of Ca2+-signalling system operating in adipocytes and integrating signals from various agonists, which describes it as multivariable multi feedback network with a family of nested positive feedback.

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Section: Resultsmentioning

confidence: 66%

Section: Resultsmentioning

confidence: 83%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Acetylcholine Promotes Ca2+and NO-Oscillations in Adipocytes Implicating Ca2+→NO→cGMP→cADP-ribose→Ca2+ Positive Feedback Loop - Modulatory Effects of Norepinephrine and Atrial Natriuretic Peptide

et al. 2013

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Cyanidin inhibits adipogenesis in 3T3-L1 preadipocytes by activating the PLC-IP3 pathway

Kongthitilerd¹,

Barras²,

Rong³

et al. 2023

Biomedicine & Pharmacotherapy

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To Break or to Brake Neuronal Network Accelerated by Ammonium Ions?

et al. 2015

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PurposeThe aim of present study was to investigate the effects of ammonium ions on in vitro neuronal network activity and to search alternative methods of acute ammonia neurotoxicity prevention.MethodsRat hippocampal neuronal and astrocytes co-cultures in vitro, fluorescent microscopy and perforated patch clamp were used to monitor the changes in intracellular Ca2+- and membrane potential produced by ammonium ions and various modulators in the cells implicated in neural networks.ResultsLow concentrations of NH4Cl (0.1–4 mM) produce short temporal effects on network activity. Application of 5–8 mM NH4Cl: invariably transforms diverse network firing regimen to identical burst patterns, characterized by substantial neuronal membrane depolarization at plateau phase of potential and high-amplitude Ca2+-oscillations; raises frequency and average for period of oscillations Ca2+-level in all cells implicated in network; results in the appearance of group of «run out» cells with high intracellular Ca2+ and steadily diminished amplitudes of oscillations; increases astrocyte Ca2+-signalling, characterized by the appearance of groups of cells with increased intracellular Ca2+-level and/or chaotic Ca2+-oscillations. Accelerated network activity may be suppressed by the blockade of NMDA or AMPA/kainate-receptors or by overactivation of AMPA/kainite-receptors. Ammonia still activate neuronal firing in the presence of GABA(A) receptors antagonist bicuculline, indicating that «disinhibition phenomenon» is not implicated in the mechanisms of networks acceleration. Network activity may also be slowed down by glycine, agonists of metabotropic inhibitory receptors, betaine, L-carnitine, L-arginine, etc.ConclusionsObtained results demonstrate that ammonium ions accelerate neuronal networks firing, implicating ionotropic glutamate receptors, having preserved the activities of group of inhibitory ionotropic and metabotropic receptors. This may mean, that ammonia neurotoxicity might be prevented by the activation of various inhibitory receptors (i.e. by the reinforcement of negative feedback control), instead of application of various enzyme inhibitors and receptor antagonists (breaking of neural, metabolic and signaling systems).

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Convergence of Ca2+ signaling pathways in adipocytes. The role of L-arginine and protein kinase G in generation of transient and periodic Ca2+ signals

Cited by 7 publications

References 42 publications

Acetylcholine Promotes Ca2+and NO-Oscillations in Adipocytes Implicating Ca2+→NO→cGMP→cADP-ribose→Ca2+ Positive Feedback Loop - Modulatory Effects of Norepinephrine and Atrial Natriuretic Peptide

Acetylcholine Promotes Ca2+and NO-Oscillations in Adipocytes Implicating Ca2+→NO→cGMP→cADP-ribose→Ca2+ Positive Feedback Loop - Modulatory Effects of Norepinephrine and Atrial Natriuretic Peptide

Cyanidin inhibits adipogenesis in 3T3-L1 preadipocytes by activating the PLC-IP3 pathway

To Break or to Brake Neuronal Network Accelerated by Ammonium Ions?

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