Submitted on March 7, 2005
Accepted on May 7, 2005
Enhanced sodium-dependent extrusion of magnesium in mutant cells established from a mouse renal tubular (MCT) cell line
Masaru Watanabe1*, Masato Konishi1, Ichiro Ohkido2, and Senya Matsufuji1
1 Department of Physiology, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan
2 Department of Biochemistry II, The Jikei University, Minato-ku, Tokyo, Japan; Division of Nephrology and Hypertension, The Jikei University, Minato-ku, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: masaru{at}tokyo-med.ac.jp.
To study the regulatory mechanisms of intracellular Mg2+ concentration ([Mg2+]i) in renal tubular cells as well as other cell types, we established a mutant strain of mouse renal cortical tubular (MCT) cells that can grow in culture media with very high Mg2+ concentrations ([Mg2+]o 100 mM: 101Mg-tolerant cells). [Mg2+]i was measured with a fluorescent indicator furaptra (mag-fura-2) in wild-type cells and the 101Mg-tolerant cells. The average level of [Mg2+]i in the 101Mg-tolerant cells was kept lower than that in the wild-type cells either at 51 mM or 1 mM [Mg2+]o. When [Mg2+]o was lowered from 51 mM to 1 mM, the decrease in [Mg2+]i was significantly faster in the 101Mg-tolerant cells than in the wild-type cells. These differences between the 101Mg-tolerant cells and the wild-type cells were abolished in the absence of extracellular Na+ or in the presence of imipramine, a known inhibitor of Na+-Mg2+ exchange. We conclude that Na+-dependent Mg2+ transport activity is enhanced in the 101Mg-tolerant cells. The enhanced Mg2+ extrusion may prevent [Mg2+]i increase to higher levels, and may be responsible for the Mg2+-tolerance.
