Zh. Liu et al., TNF-ALPHA AND IL-1-ALPHA INDUCE MANNOSE RECEPTORS AND APOPTOSIS IN GLOMERULAR MESANGIAL BUT NOT ENDOTHELIAL-CELLS, American journal of physiology. Cell physiology, 39(6), 1996, pp. 1595-1601
The macrophage mannose receptor, a carbohydrate-binding membrane prote
in, mediates endocytosis and phagocytosis. This study was undertaken t
o determine whether mannose receptors were expressed in resting glomer
ular mesangial and endothelial cells and whether their level was affec
ted by cytokines. Neither mannose receptor mRNA nor proteins were foun
d in resting mesangial or endothelial cells. Mannose receptor mRNA was
induced in a dose- and time-dependent manner in mesangial cells by in
terleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alp
ha) but not by platelet-derived growth factor-B or IL-6. Cell surface
receptors were found by fluorescence-activated cell sorter analysis. B
inding to stimulated mesangial cells was saturable and inhibited by ex
cess mannose-bovine serum albumin (BSA) but not by galactose-BSA. TNF-
alpha and IL-1 alpha also induced apoptosis in mesangial cells. Mannos
e receptor expression was not restricted to apoptotic stimulated mesan
gial cells. Neither agonist induced mannose receptor expression or apo
ptosis in endothelial cells. Because immunoglobulin A, M, and G contai
n mannose residues, immune aggregates may be removed from the mesangiu
m through cytokine-induced mannose receptors.