{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,10]],"date-time":"2025-12-10T12:11:15Z","timestamp":1765368675881},"reference-count":29,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,11,3]],"date-time":"2009-11-03T00:00:00Z","timestamp":1257206400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mammary epithelial cells (HC11) chronically adapted to grow in a low\u2010magnesium (0.05\u2009mM vs. 0.5\u2009mM) or in a high\u2010magnesium (40\u2009mM) medium were used to investigate on the mechanisms of cell magnesium transport under conditions of non\u2010physiological magnesium availability. Magnesium influx was higher in low\u2010magnesium cells compared to control or high\u2010magnesium cells, whereas magnesium efflux was higher in high\u2010magnesium cells compared to control and low\u2010magnesium cells. Magnesium efflux was partially inhibited by imipramine, inhibitor of the Na<jats:sup>+<\/jats:sup>\/Mg<jats:sup>2+<\/jats:sup> exchange. Using a monoclonal antibody detecting a \u223c70\u2009kDa protein associated with Na<jats:sup>+<\/jats:sup>\/Mg<jats:sup>2+<\/jats:sup> exchange activity, we found that the expression levels of this protein were proportional to magnesium efflux capacity, that is, high\u2010magnesium cells\u2009&gt;\u2009control cells\u2009&gt;\u2009low\u2010magnesium cells. As for magnesium influx, this was abolished by Co(III)hexaammine, inhibitor of magnesium channels. Surprisingly, we found that cells grown in low magnesium upregulated mRNA for the magnesium channel TRPM6, but not for other channels like TRPM7 or MagT1. TRPM6 mRNA was also rapidly upregulated or downregulated in HC11 cells deprived of magnesium or in low\u2010magnesium cells re\u2010added with magnesium, respectively. TRPM6 protein levels, as assessed by Western blot and immunofluorescence, underwent similar changes under comparable conditions. We propose that mammary epithelial cells adapt to decreased magnesium availability by upregulating magnesium influx via TRPM6, and counteract increased magnesium availability by increasing magnesium efflux primarily via Na<jats:sup>+<\/jats:sup>\/Mg<jats:sup>2+<\/jats:sup> exchange. These results show, for the first time, that TRPM6 contributes to regulating magnesium influx in mammary epithelial cells, similar to what is known for intestine and kidney. J. Cell. Physiol. 222: 374\u2013381, 2010. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21961","type":"journal-article","created":{"date-parts":[[2009,11,3]],"date-time":"2009-11-03T22:51:10Z","timestamp":1257288670000},"page":"374-381","source":"Crossref","is-referenced-by-count":22,"title":["Modulation of TRPM6 and Na<sup>+<\/sup>\/Mg<sup>2+<\/sup> exchange in mammary epithelial cells in response to variations of magnesium availability"],"prefix":"10.1002","volume":"222","author":[{"given":"Federica 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