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*
Centre for Inflammation Research, Department of Clinical and Surgical Sciences (Internal Medicine), Royal Infirmary, University of Edinburgh, Edinburgh, United Kingdom;
Department of Immunology, University of Glasgow, Glasgow, United Kingdom; and
Department of Medicine and Therapeutics, University of Aberdeen, Foresterhill, Aberdeen, United Kingdom
During inflammation in the glomerulus, the complement of resident
myofibroblast-like mesangial cells is regulated by mitosis and
apoptosis, but the cellular mechanisms controlling the size of
mesangial cell populations have remained obscure. Prompted by studies
of development, we sought evidence that macrophages regulate mesangial
cell number. Rat bone marrow-derived macrophages primed with IFN-
then further activated in coculture with LPS or TNF-
elicited a
10-fold induction of rat mesangial cell apoptosis and complete
suppression of mitosis, effects inhibitable by the NO synthase
inhibitors L-monomethyl arginine and
L-N6-(1-iminoethyl) lysine
dihydrochloride. Complete dependence upon macrophage-derived NO was
observed in comparable experiments employing activated bone marrow
macrophages from wild-type and NO synthase 2-/- mice.
Nevertheless, when mesangial cells were primed with IFN- plus
TNF-, increased induction by activated macrophages of mesangial
apoptosis exhibited a NO-independent element. The use of
gld/gld macrophages excluded a role for Fas ligand in
this residual kill, despite increased expression of Fas and increased
susceptibility to soluble Fas ligand exhibited by cytokine-primed
mesangial cells. Finally, activated macrophages isolated from the
glomeruli of rats with nephrotoxic nephritis also induced apoptosis and
suppressed mitosis in mesangial cells by an L-monomethyl
arginine-inhibitable mechanism. These data demonstrate that activated
macrophages, via the release of NO and other mediators, regulate
mesangial cell populations in vitro and may therefore control the
mesangial cell complement at inflamed sites.
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