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http://purl.uniprot.org/citations/26355001http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26355001http://www.w3.org/2000/01/rdf-schema#comment"

Background

Magnesium deficiency is a common complication of diabetes with an unclear molecular background.

Objective

We investigated the effect of the insulin (INS)-signaling pathway (ISP) on the regulation of Mg(2+) efflux (Mg(2+)E) conducted by solute carrier family 41, member A1 (SLC41A1; activated by protein kinase A) in transgenic human embryonic kidney (HEK) 293 cells.

Methods

HEK293 cells overexpressing SLC41A1 were loaded with the Mg(2+) fluorescent indicator mag-fura-2 and Mg(2+). Measurements of Mg(2+)E were conducted in Mg(2+)-free buffer by using fast-filter fluorescence spectrometry. We examined the effects of INS, inhibitors of ISP or p38 mitogen-activated protein kinase (p38 MAPK), an activator of adenylate cyclase (ADC), and their combinations on SLC41A1-attributed Mg(2+)E.

Results

The application of 400 μU/mL INS inhibited SLC41A1-mediated Mg(2+)E by up to 50.6% compared with INS-untreated cells (P < 0.001). Moreover, INS evoked the early onset of Mg(2+) release from intracellular stores. The application of 0.1 μM wortmannin or 10 μM zardaverine (both ISP inhibitors) restored SLC41A1 Mg(2+)E capacity in the presence of INS to the same levels in INS-untreated cells. The simultaneous application of 10 μM forskolin, an ADC activator, and INS resulted in a reduction of Mg(2+)E of up to 59% compared with untreated cells (P < 0.001), which was comparable to that in cells treated with INS alone. Inhibition of p38 MAPK with 10 μM SB 202190 (SB) in the absence of INS resulted in a decrease (P < 0.001) of SLC41A1-dependent Mg(2+)E (by up to 49%) compared with Mg(2+)E measured in untreated cells. Simultaneous exposure of cells to SB and INS had a stronger inhibitory effect on SLC41A1 activity than INS alone (P < 0.05).

Conclusions

INS affects intracellular Mg(2+) concentration in transgenic HEK293 cells by regulating SLC41A1 activity (via ISP) and by influencing the compartmentalization and cellular distribution of Mg(2+). In addition, p38 MAPK activates SLC41A1 independently of INS action."xsd:string
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http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Sponder G."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Kolisek M."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Aschenbach J.R."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Mastrototaro L."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Vormann J."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/author"Tietjen U."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/name"J Nutr"xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/pages"2440-2447"xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/title"Insulin Modulates the Na+/Mg2+ Exchanger SLC41A1 and Influences Mg2+ Efflux from Intracellular Stores in Transgenic HEK293 Cells."xsd:string
http://purl.uniprot.org/citations/26355001http://purl.uniprot.org/core/volume"145"xsd:string
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