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CD36 Mediates Proximal Tubular Binding and Uptake of Albumin and is Up-Regulated in Proteinuric Nephropathies.


Am J Physiol Renal Physiol. 2012 Jul 11;


Authors: Baines RJ, Chana RS, Hall M, Febbraio M, Kennedy DJ, Brunskill NJ


Abstract

Dysregulation of renal tubular protein handling in proteinuria contributes to the development of chronic kidney disease. We investigated the role of CD36 as a novel candidate mediator of albumin binding and endocytosis in the kidney proximal tubule using both in-vitro and in-vivo approaches, and in nephrotic patient renal biopsy samples. In CD36 transfected opossum kidney proximal tubular cells, both binding and uptake of albumin were substantially enhanced. A specific CD36 inhibitor abrogated this effect, but receptor-associated protein, which blocks megalin mediated endocyotsis of albumin, did not. Mouse proximal tubular cells expressed CD36 and this was absent in CD36 null animals, whereas expression of megalin was equal in these animals. When compared to wild type mice, CD36 null mice demonstrated a significantly increased urinary protein:creatinine ratio and albumin:creatinine ratio. Proximal tubular cells expressed increased CD36 when exposed to elevated albumin concentrations in culture medium. Expression of CD36 was studied in renal biopsy tissue obtained from adult patients with heavy proteinuria due to minimal change disease, membranous nephropathy or focal segmental glomerulosclerosis. Proximal tubular CD36 expression was markedly increased in proteinuric individuals. We conclude that CD36 is a novel mediator influencing binding and uptake of albumin in the proximal tubule that is upregulated in proteinuric renal diseases. CD36 may represent a potential therapeutic target in proteinuric nephropathy.

PMID: 22791331 [PubMed - as supplied by publisher]