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First published online October 27, 2005

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Tight junction for magnesium

In multicellular organisms, compartments with different compositions are separated by epithelia. Exchange of solutes between compartments can occur through (transcellular) or around (paracellular) the epithelial cells. Tight junctions between the cells form an ion-selective barrier across the paracellular route, and several human diseases involve a breakdown of these junctions. On p. 5109, Daniel Goodenough and colleagues report that the tight junction protein paracellin 1 (claudin-16) can modulate tight junction ion selectivity in the renal epithelial cell line LLC-PK1, which does not normally express this protein. When the authors express paracellin 1 in these cells, it localizes to the tight junctions and increases their permeability to Na⁺ but not to Cl^- or Mg²⁺. Mutagenesis studies indicated that the extracellular loops of paracellin 1 are critical for this ion selectivity. Similar paracellin 1 mutations cause human familial hypomagnesemia with hypocalcinuria and nephrocalcinosis (FHHNC), which is characterised by Mg²⁺ wasting. Mg²⁺ reabsorption in the kidneys is normally driven by a lumen-positive voltage in the thick ascending limb of the nephron; so the authors propose that, in FHHNC, paracellin 1 mutations dissipate this voltage, thus reducing Mg²⁺ reabsorption.

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Related articles in JCS:

Paracellin-1 and the modulation of ion selectivity of tight junctions

Jianghui Hou, David L. Paul, and Daniel A. Goodenough
JCS 2005 118: 5109-5118. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?