Na+/Mg2+ transporter acts as a Mg2+ buffering mechanism in PC12 cells

Kubota, Takeshi; Tokuno, Kentaro; Nakagawa, Jun; Kitamura, Yoshiichiro; Ogawa, Hiroto; Suzuki, Yoshio; Suzuki, Kôji; Oka, Kotaro

doi:10.1016/s0006-291x(03)00346-2

Cited by 24 publications

(16 citation statements)

References 26 publications

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“…Our results are also consistent with numerous experimental observations including work by Flatman et al [35] and Kubota et al, [25,26] with fluorescent indicators indicating a persistent elevation in cytosolic free [Mg 2+ ] i under conditions in which extracellular Na + is not available to favor Mg 2+ extrusion. The specific inhibition of Mg 2+ extrusion by imipramine or quinidine, two agents reported to block the Na + -dependent Mg 2+ transport in a variety of cells [11,36], further indicates that the extrusion of Mg 2+ induced by the addition of cyanide occurs through a specific transport mechanism.…”

Section: Discussionsupporting

confidence: 93%

“…Previous observation from this and other laboratories indicate that cellular Mg 2+ is extruded across the plasma membrane of liver cells through a Na + -dependent and a Na + -independent mechanism under a variety of hormonal stimuli or experimental conditions [4,5,7,25,26]. The possibility that the cyanide-induced Mg 2+ extrusion occurred via either mechanism was investigated by selectively modifying the cation composition of the extracellular medium [27].…”

Section: Resultsmentioning

confidence: 99%

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Adenosine triphosphate depletion by cyanide results in a Na+-dependent Mg2+ extrusion from liver cells

Dalal

Romani

2010

Metabolism

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Addition of NaCN to isolated hepatocytes results in a marked and rapid decrease in cellular ATP content, and in the extrusion of a sizable amount of cellular Mg2+. This extrusion starts after a 10 min lag phase and reaches a maximum of 35 to 40 nmol Mg2+/mg protein within 60 min from the addition of CN−. A quantitatively similar Mg2+ extrusion is also observed following the addition of the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP) but not that of the glycolysis inhibitor iodoacetate. The Mg2+ extrusion is completely inhibited by the removal of extracellular Na+ or the addition of imipramine, quinidine or glibenclamide, while it persists following the removal of extracellular Ca2+ or K+, or the addition of amiloride. An acidic extracellular pH or the removal of extracellular HCO3− inhibits the cyanide-induced Mg2+ extrusion by ≥80%. Taken together, these data suggest that the decrease in cellular ATP content removes a major Mg2+ complexing agent from the hepatocyte, and results in an extrusion of hepatic Mg2+ exclusively through a Na+-dependent exchange mechanism modulated by acidic changes in extracellular pH.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Adenosine triphosphate depletion by cyanide results in a Na+-dependent Mg2+ extrusion from liver cells

Dalal

Romani

2010

Metabolism

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“…The A1-related Mg 2+ extrusion was not directly linked to anion (Cl − , HCO 3 − ) transport. However, it showed typical features of NME such as 1) activation by an increased [Mg 2+ ] i [26], 2) strict dependence on extracellular Na + [31, 32], 3) inhibition by imipramine and quinidine [33] and, 4) regulation via cAMP-dependent PKA [33]. Thus, unquestionably, A1 represents NME, the predominant Mg 2+ efflux system in mammalian cells [32, 34].…”

Section: Slc41a1 As a Na+/mg2+ Exchangermentioning

confidence: 99%

Solute carrier family SLC41: what do we really know about it?

Fleig

Schweigel-Röntgen

Kolísek

2013

WIREs Membr Transp Signal

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The 41st family of solute carriers (SLC41) comprises three members A1, A2 and A3, which are distantly homologous to bacterial Mg2+ channel MgtE. SLC41A1 was recently characterized as being an Na+/Mg2+ exchanger (NME; a predominant cellular Mg2+ efflux system). Little is known about the exact function of SLC41A2 and SLC41A3, although, these proteins have also been linked to Mg2+ transport in human (animal) cells. The molecular biology (including membrane topology, cellular localization, transcriptomics and proteomics) of SLC41A2 and SLC41A3 compared with SLC41A1 has only been poorly explored. Significantly more data with regard to function, functional regulation, involvement in cellular signalling, complex-forming ability, spectrum of binding partners and involvement in the pathophysiology of human diseases are available for SLC41A1. Three recent observations namely the identification of the null mutation, c.698G>T, in SLC41A1 underlying the nephronophthisis-like phenotype, the recognition of a putative link between SLC41A1 and Parkinson’s disease, and the observation that nearly 55% of preeclamptic placental samples overexpress SLC41A1, marks the protein as a possible therapeutic target of these diseases. A potential role of the SLC41 family of Mg2+ transporters in the pathophysiology of human diseases is further substantiated by the finding that SLC41A3 knockout mice develop abnormal locomotor coordination.

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“…While a detailed account on the application of the aforementioned probes is beyond the scope of this review, a few examples are given which indicate the potential of these synthetic fluorescent probes as ion indicators: The use of BTC and MCC-type probes in investigations of Ca 2+ -dependent exocytosis [19], and rates of K + transport across biological membranes [54], respectively. The monitoring of K + efflux from Sf 9 and Cf1 insect cells using CD-222 [55], the applicability of crown ether derivatives such as C343-crown in ion detection [56], the potential use of 4-(monoaza-18-crown-6-methyl)-7-octadecanoylaminocoumarin in optical fiber fluorescence sensor for the detection of saxitoxin [57], the real-time detection of phosphodiesterase 3':5'-cyclic mononucleotide activity by the Cd 2+ -cylen type anion probe [58], and the demonstration of Mg 2+ buffering mechanisms in PC12 cells using KMG-20 [59].…”

Section: Miscellaneous Coumarin Fluorescent Ion Indicatorsmentioning

confidence: 99%

The Coumarin Moiety as Chromophore of Fluorescent Ion Indicators in Biological Systems

Katerinopoulos

2004

CPD

120

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Fluorescent probes have evolved into an extremely useful tool for the detection of ions in biological systems. The design of ion indicators is based in the proper choice of the ion chelating group as well as the chromophore moiety. The chromophores of choice should fulfill a number of requirements concerning the photostability of the group, the range of the excitation and emission wavelengths of the indicators, the Stokes shift, the fluorescence quantum yield, the excitation and/or emission wavelength shift upon coordination of the probe with its target ion, the lipophilicity of the indicators, and their possible cell toxicity. Coumarin and its analogues have been extensively used in ion detection by incorporation of the coumarin chromophore in the larger indicator framework. Coumarins fulfill all the aforementioned requirements since they are relatively photostable and their excitation and emission maxima, in many cases, are long enough to minimise "background" fluorescence of cellular components, tissues and biological fluids. They exhibit Stokes shifts large enough to avoid significant overlap of the excitation and emission spectra, their fluorescence quantum yields allow for ion detection at low indicator concentrations, and they can be introduced to cells either by microinjection or as membrane permeable derivatives without causing cell death. Synthetic approaches, aiming at the optimisation of indicator properties, have extended the conjugated coumarin system either by introduction of substituents or by expansion of the heterocyclic system. In this review, the basic rationale for the selection of the particular coumarin analogues is analysed, synthetic pathways leading to the desired structures are presented, and properties and relative advantages in the use of these probes are described.

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Na+/Mg2+ transporter acts as a Mg2+ buffering mechanism in PC12 cells

Cited by 24 publications

References 26 publications

Adenosine triphosphate depletion by cyanide results in a Na+-dependent Mg2+ extrusion from liver cells

Adenosine triphosphate depletion by cyanide results in a Na+-dependent Mg2+ extrusion from liver cells

Solute carrier family SLC41: what do we really know about it?

The Coumarin Moiety as Chromophore of Fluorescent Ion Indicators in Biological Systems

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