albumin - publications

Predict more albumin - ligand interactions now!

1. Nephron Exp Nephrol. 2012 May 16;120(3):e91-e102. [Epub ahead of print]

Albumin-Induced Epithelial Mesenchymal Transformation.

Ibrini J, Fadel S, Chana RS, Brunskill N, Wagner B, Johnson TS, El Nahas AM.

Sheffield Kidney Institute and Academic Nephrology Unit, University of Sheffield,
Sheffield, UK.

Background: Progressive chronic kidney disease is often associated with
albuminuria and renal fibrosis linked to the accumulation of myofibroblasts
producing extracellular matrix. Renal myofibroblasts are derived from a number of
cells including tubular epithelial cells (TECs) through epithelial mesenchymal
transformation (EMT). This study explores the hypothesis that exposure of TECs to
albumin induces EMT. Methods: Normal rat TECs (NRK52E) were exposed in culture to
de-lipidated bovine serum albumin (dBSA; 10 mg/ml) for 2, 4 and 6 days.
Binding/uptake of fluoresceined albumin by PTCs was evaluated. Transformation
into myofibroblasts was assessed by light and electron microscopy,
immunofluorescence and Western blotting for α-smooth muscle actin (α-SMA),
E-cadherin and transforming growth factor-β1 (TGF-β1). We also investigated the
expression of fibroblast-specific protein-1 (FSP-1) and collagens I, III and IV.
TGF-β1 biological activity, mRNA and protein were measured. A neutralising
anti-TGF-β1 antibody was used to analyse the role of TGF-β1 in albumin-induced
EMT. Results: Exposure of TECs to dBSA led to binding/uptake of albumin as well
as fibroblastic morphological changes. Incubation of TECs with dBSA caused a
reduction of TEC marker E-cadherin (ANOVA p = 0.0002) and de novo expression of
fibroblast markers α-SMA and FSP-1 (ANOVA p = 0.0001) in a time-dependent manner.
It also increased expression and activity of TGF-β1. Neutralisation of TGF-β1
significantly reduced EMT (p < 0.01). Conclusion: This study demonstrates that in
vitro, albumin induces the transformation of TECs into cells with myofibroblast
characteristics; a process that may be TGF-β1 dependent.

Copyright © 2012 S. Karger AG, Basel.

PMID: 22613868 [PubMed - as supplied by publisher]