TNF-ALPHA AND IL-1-ALPHA INDUCE MANNOSE RECEPTORS AND APOPTOSIS IN GLOMERULAR MESANGIAL BUT NOT ENDOTHELIAL-CELLS

Citation
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
Citations number
30
Categorie Soggetti
Physiology
ISSN journal
03636143
Volume
39
Issue
6
Year of publication
1996
Pages
1595 - 1601
Database
ISI
SICI code
0363-6143(1996)39:6<1595:TAIIMR>2.0.ZU;2-K
Abstract
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.