Tnf-[alpha] and il-1[alpha] induce mannose receptors and apoptosis
in glomerular mesangial but not endothelial cells .
Liu, Zhi-Hong, Gary E. Striker, Maryalice Stetler-Stevenson, Paula
Fukushima, Aneeta Patel, and Liliane J. Striker.
Renal Cell Biology Section, Metabolic Diseases Branch, National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health, Bethesda, MD 20892-1268, Flow Cytomety Unit,
Laboratory of Pathology, National Cancer Institute, National
Institute of Health, Bethesda, MD 20982
APStracts 2:0428C, 1995.
The macrophage mannose receptor, a carbohydrate-binding membrane
protein, mediates endocytosis and phagocytosis. This study was
undertaken to determine if mannose receptors were expressed in
resting glomerular mesangial and endothelial cells, and whether their
level was affected by cytokines. Neither mannose receptor mRNA nor
proteins were found in resting mesangial or endothelial cells.
Mannose receptor mRNA was induced in a dose and time-dependent manner
in mesangial cells by IL-1[alpha] or TNF-[alpha], but not by PDGF-B
or IL-6. Cell surface receptors were found by FACS analysis. Binding
to stimulated mesangial cells was saturable and inhibited by excess
mannose-BSA, but not by galactose-BSA. TNF-[alpha] and IL-1[alpha]
also induced apoptosis in mesangial cells. Mannose receptor
expression was not restricted to apoptotic, stimulated mesangial
cells. Neither agonist induced mannose receptor expression or
apoptosis in endothelial cells. Since IgA, IgM, and IgG contain
mannose residues, immune aggregates may be removed from the mesangium
through cytokine-induced mannose receptors.
Received 4 August 1995; accepted in final form 17 November 1995.
APS Manuscript Number C480-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95