Journal
FEBS LETTERS
Volume 582, Issue 5, Pages 611-615Publisher
WILEY
DOI: 10.1016/j.febslet.2008.01.025
Keywords
uteroglobin; Clara cell 10 kDa protein; fibronectin; IgA-nephropathy
Funding
- Intramural NIH HHS [Z99 HD999999, Z01 HD000910-28] Funding Source: Medline
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Immunoglobulin A (IgA)-nephropathy (IgAN) is the most common primary renal glomerular disease in the world that has no effective treatment. High levels of circulating IgA-fibronectin (Fn) complexes, characteristically found in IgAN patients, are suggested to cause abnormal deposition of IgA and Fn in the renal glomeruli of these patients causing renal failure. We previously reported that binding of Fn to uteroglobin (UG), a multifunctional anti-inflammatory protein, inhibits Fn-IgA heteromerization. However, the specific site of Fn-UG interaction until now remained unidentified. We report here that UG interacts with the heparin-binding site of Fn and propose that small molecules competing for interaction with this site may reduce the level of circulating Fn-IgA complexes in IgAN. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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