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Dual action of neutrophil gelatinase-associated lipocalin

Item Type:Article
Title:Dual action of neutrophil gelatinase-associated lipocalin
Creators Name:Schmidt-Ott, K.M. and Mori, K. and Li, J.Y. and Kalandadze, A. and Cohen, D.J. and Devarajan, P. and Barasch, J.
Abstract:Neutrophil gelatinase-associated lipocalin (NGAL) is expressed and secreted by immune cells, hepatocytes, and renal tubular cells in various pathologic states. NGAL exerts bacteriostatic effects, which are explained by its ability to capture and deplete siderophores, small iron-binding molecules that are synthesized by certain bacteria as a means of iron acquisition. Consistently, NGAL deficiency in genetically modified mice leads to an increased growth of bacteria. However, growing evidence suggests effects of the protein beyond fighting microorganisms. NGAL acts as a growth and differentiation factor in multiple cell types, including developing and mature renal epithelia, and some of this activity is enhanced in the presence of siderophore:iron complexes. This has led to the hypothesis that eukaryotes might synthesize siderophore-like molecules that bind NGAL. Accordingly, NGAL-mediated iron shuttling between the extracellular and intracellular spaces may explain some of the biologic activities of the protein. Interest in NGAL has been sparked by the observation that NGAL is massively upregulated after renal tubular injury and may participate in limiting kidney damage. This review summarizes the current knowledge about the dual effects of NGAL as a siderophore:iron-binding protein and as a growth factor and examines the role of these effects in renal injury.
Keywords:Acute-Phase Proteins, Animal Models, Carrier Proteins, Cell Differentiation, Iron, Kidney, Kidney Diseases, Kidney Tubules, Lipocalins, Neutrophils, Proto-Oncogene Proteins, Signal Transduction, Animals, Mice
Source:Journal of the American Society of Nephrology
Publisher:American Society of Nephrology
Page Range:407-413
Date:February 2007
Official Publication:https://doi.org/10.1681/ASN.2006080882
PubMed:View item in PubMed

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