Differentiation of HL-60 promyelocytic leukemia cells is accompanied by a modification of magnesium homeostasis

✍ Scribed by F.I. Wolf; V. Covacci; N. Bruzzese; A. Di Francesco; A. Sacchetti; D. Corda; A. Cittadini

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 121 KB
• Volume: 71
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/(sici)1097-4644(19981201)71:3<441::aid-jcb12>3.0.co;2-o

✦ Synopsis

Magnesium homeostasis in HL-60 promyelocytic leukemia cells was compared to that in neutrophyllike HL-60 cells obtained by 1.3% DMSO treatment. Magnesium homeostasis was studied by the characterization of magnesium efflux, the identification of intracellular magnesium pools, and the regulation of intracellular ionized Mg 2ϩ . In both undifferentiated and neutrophyl-like HL-60 cells, magnesium efflux occurred via the Na-Mg antiporter which was inhibited by imipramine and stimulated by db cAMP and forskolin. Receptor-mediated signals such as ATP, IFN-␣, or PGE1, which can trigger cAMP-dependent magnesium efflux, were ineffective in undifferentiated HL-60 cells but induced 60-70% increase of magnesium efflux in neutrophyl-like HL-60 cells. Selective membrane permeabilization by the cation ionophore A23187 induced a large magnesium release when cells were treated with rotenone. In both cell populations, the addition of glucose to rotenone-treated cells restored magnesium release to the control level. Permeabilization by 0.005% digitonin provoked the release of 90% cell total magnesium in both cell types. Intracellular [Mg 2ϩ ] i was 0.15 and 0.26 mM in undifferentiated and neutrophyl-like HL-60 cells, respectively. Stimuli that triggered magnesium efflux, such as db cAMP in undifferentiated and IFN-␣ in neutrophyl-like HL-60 cells, induced a slow but consistent increase of [Mg 2ϩ ] i which was independent from Ca 2ϩ movements. Overall, these data indicate that magnesium homeostasis is regulated by receptor-mediated magnesium efflux which was modified during differentiation of HL-60 cells. Stimulation of magnesium efflux is paralleled by an increase of [Mg 2ϩ ] i which reflects a release of magnesium from the bound cation pool.