When EGF is offside, magnesium is wasted

J Clin Invest. 2007 Aug;117(8):2086-9. doi: 10.1172/JCI33004.

Abstract

Our understanding of magnesium (Mg(2+)) regulation has recently been catapulted forward by the discovery of several disease loci for monogenic disorders of Mg(2+) homeostasis. In this issue of the JCI, Groenestege et al. report that their study of a rare inherited Mg(2+) wasting disorder in consanguineous kindred shows that EGF acts as an autocrine/paracrine magnesiotropic hormone (see the related article beginning on page 2260). EGF stimulates Mg(2+) reabsorption in the renal distal convoluted tubule (DCT) via engagement of its receptor on the basolateral membrane of DCT cells and activation of the Mg(2+) channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) in the apical membrane. These authors show that a point mutation in pro-EGF retains EGF secretion to the apical but not the basolateral membrane, disrupting this cascade and causing renal Mg(2+) wasting. This work is another seminal example of the power of the study of monogenic disorders in the quest to understand human physiology.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Animals
  • Antibodies, Monoclonal / adverse effects
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / therapeutic use
  • Cetuximab
  • Colorectal Neoplasms / complications
  • Colorectal Neoplasms / drug therapy
  • Epidermal Growth Factor / genetics*
  • Epidermal Growth Factor / metabolism*
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Female
  • Humans
  • Kidney / metabolism
  • Magnesium / metabolism*
  • Male
  • Mutation*
  • Pedigree
  • Protein Precursors / genetics*
  • Protein Precursors / metabolism*
  • Protein Processing, Post-Translational / drug effects
  • Protein Processing, Post-Translational / genetics*
  • Renal Tubular Transport, Inborn Errors / chemically induced
  • Renal Tubular Transport, Inborn Errors / genetics*
  • Renal Tubular Transport, Inborn Errors / metabolism*
  • TRPM Cation Channels / biosynthesis
  • TRPM Cation Channels / genetics
  • Tetany / chemically induced
  • Tetany / genetics
  • Tetany / metabolism

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents
  • Protein Precursors
  • TRPM Cation Channels
  • TRPM6 protein, human
  • epidermal growth factor precursor
  • Epidermal Growth Factor
  • EGFR protein, human
  • ErbB Receptors
  • Magnesium
  • Cetuximab