Nephrology Dialysis Transplantation, Vol 13, Issue 1 37-43, Copyright © 1998 by Oxford University Press
T Jocks, J Freudenberg, G Zahner and R Stahl
These studies were designed to determine the possible role of
platelet-activating factor (PAF) in the production of monocyte
chemoattractant protein-1 (MCP-1) in glomerular immune injury. The
glomerular lesion was induced in isolated perfused rat kidneys by a rabbit
anti-rat-thymocyte serum (ATS) and rat serum (RS) as a complement source.
Perfusion of kidneys with ATS and RS results in the selective binding of
the antiserum to the glomerular mesangium with consecutive intraglomerular
activation of complement. Antibody binding and complement activation
induced a significant increase in glomerular MCP-1 mRNA levels when
assessed by Northern blotting or RT-PCR. Decomplemented RS or non antibody
rabbit IgG had only moderate effects on glomerular MCP-1 mRNA levels. The
PAF receptor antagonist WEB 2170 almost completely blocked the ATS and RS
induced MCP-1 mRNA levels. Perfusion of control kidneys with PAF increased
MCP-1 mRNA expression, an effect which was blocked by WEB 2170. Glomerular
MCP-1 protein formation, assessed by Western blotting, was stimulated
following ATS and RS and PAF, respectively, was blocked by WEB 2170. These
data show that PAF, derived from glomerular resident cells following
antibody and complement induced injury, stimulates MCP-1 expression. In
addition to the direct effects on leukocyte adhesion and activation PAF may
mediate inflammatory cell influx in glomerular injuries due to the release
of MCP-1. Key words: glomerular immune injury;
isolated perfused kidney; monocyte chemoattractant protein-1; platelet
activating factor
ORIGINAL ARTICLES
Platelet-activating factor mediates monocyte chemoattractant protein-1 expression in glomerular immune injury
Department of Medicine, Division of Nephrology, Pa. 61, University Hospital Eppendorf (UKE), Martinistr. 52, D-20246 Hamburg, Germany
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