albumin - publications

Predict more albumin - ligand interactions now!


1. PLoS One. 2012;7(2):e31388. Epub 2012 Feb 3.

Homocysteinylated Albumin Promotes Increased Monocyte-Endothelial Cell Adhesion
and Up-Regulation of MCP1, Hsp60 and ADAM17.

Capasso R, Sambri I, Cimmino A, Salemme S, Lombardi C, Acanfora F, Satta E,
Puppione DL, Perna AF, Ingrosso D.

Department of Biochemistry and Biophysics "F. Cedrangolo", School of Medicine,
Second University of Naples, Naples, Italy.

RATIONALE: The cardiovascular risk factor homocysteine is mainly bound to
proteins in human plasma, and it has been hypothesized that homocysteinylated
proteins are important mediators of the toxic effects of hyperhomocysteinemia. It
has been recently demonstrated that homocysteinylated proteins are elevated in
hemodialysis patients, a high cardiovascular risk population, and that
homocysteinylated albumin shows altered properties.
OBJECTIVE: Aim of this work was to investigate the effects of homocysteinylated
albumin - the circulating form of this amino acid, utilized at the concentration
present in uremia - on monocyte adhesion to a human endothelial cell culture
monolayer and the relevant molecular changes induced at both cell levels.
METHODS AND RESULTS: Treated endothelial cells showed a significant increase in
monocyte adhesion. Endothelial cells showed after treatment a significant,
specific and time-dependent increase in ICAM1 and VCAM1. Expression profiling and
real time PCR, as well as protein analysis, showed an increase in the expression
of genes encoding for chemokines/cytokines regulating the adhesion process and
mediators of vascular remodeling (ADAM17, MCP1, and Hsp60). The mature form of
ADAM17 was also increased as well as Tnf-α released in the cell medium. At
monocyte level, treatment induced up-regulation of ICAM1, MCP1 and its receptor
CCR2.
CONCLUSIONS: Treatment with homocysteinylated albumin specifically increases
monocyte adhesion to endothelial cells through up-regulation of effectors
involved in vascular remodeling.

PMID: 22319627 [PubMed - in process]