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Am J Physiol Renal Physiol 285: F9-F18, 2003; doi:10.1152/ajprenal.00008.2003
0363-6127/03 $5.00
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INVITED REVIEW

Iron, lipocalin, and kidney epithelia

Jun Yang, Kiyoshi Mori, Jau Yi Li, and Jonathan Barasch

Department of Medicine and Anatomy and Cell Biology, College of Physicians and Surgeons of Columbia University, New York, New York 10032

Brilliant new discoveries in the field of iron metabolism have revealed novel transmembrane iron transporters, novel hormones that regulate iron traffic, and iron's control of gene expression. An important role for iron in the embryonic kidney was first identified by Ekblom, who studied transferrin (Landschulz W and Ekblom P. J Biol Chem 260: 15580–15584, 1985; Landschulz W, Thesleff I, and Ekblom P. J Cell Biol 98: 596–601, 1984; Thesleff I, Partanen AM, Landschulz W, Trowbridge IS, and Ekblom P. Differentiation 30: 152– 158, 1985). Nevertheless, how iron traffics to developing organs remains obscure. This review discusses a member of the lipocalin superfamily, 24p3 or neutrophil gelatinase-associated lipocalcin (NGAL), which induces the formation of kidney epithelia. We review the data showing that lipocalins transport low-molecular-weight chemical signals and data indicating that 24p3/NGAL transports iron. We compare 24p3/NGAL to transferrin and a variety of other iron trafficking pathways and suggest specific roles for each in iron transport.

metanephric mesenchyme; induction; neutrophil gelatinase-associated lipocalin; NGAL; 24p3; transferrin; embryo


Address for reprint requests and other correspondence: J. Barasch, Dept. of Medicine and Anatomy and Cell Biology, College of Physicians and Surgeons of Columbia Univ., 630 W 168th St., New York, NY 10032 (E-mail: jmb4{at}columbia.edu).




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