TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells

Abstract

The macrophage mannose receptor, a carbohydrate-binding membrane protein, mediates endocytosis and phagocytosis. This study was undertaken to determine whether 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 interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. Cell surface receptors were found by fluorescence-activated cell sorter analysis. Binding to stimulated mesangial cells was saturable and inhibited by excess mannose-bovine serum albumin (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. Because immunoglobulin A, M, and G contain mannose residues, immune aggregates may be removed from the mesangium through cytokine-induced mannose receptors.

Correlation between Sustained c-Jun N-terminal Protein Kinase Activation and Apoptosis Induced by Tumor Necrosis Factor-α in Rat Mesangial Cells

“…Although it is reported that cycloheximide by itself activates JNK in some cells (15), its effect on mesangial cells was rather weak. A similar result was also reported by Liu et al in rat mesangial cells (34).…”

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

“…Meanwhile, inflammatory reaction and cytokines (TNF-α and IL-6) will be produced by slowing enterocinesia, injuring intestinal epithelial, bacteria adhesion and penetration of intestinal epithelium, and induce and regulate intestinal epithelial apoptosis (Ikeda et al, 1998). Besides, the linkage between epithelial cell and cell matrix will be damaged by abnormal expression of cellular adhesion molecule (Swank et al, 1998) while the apoptosis in vivo or in vitro will also be increased by excessive inflammatory cytokines such as TNF-α and IL-1β (Dunger et al, 1996;Liu et al, 1996).…”

Selective Sensitization to Tumor Necrosis Factor-α-induced Apoptosis by Blockade of NF-κB in Primary Glomerular Mesangial Cells

“…Mutant IB␣ Does Not Sensitize Mesangial Cells to Apoptosis Induced by Other Stimuli-Because our data indicated that a blockade of NF-B by IB␣M sensitized mesangial cells to apoptosis induced by TNF-␣ but had no sensitizing effect toward proapoptotic serum deprivation or to IL-1␤ and IL-1␣, which can induce mesangial cell apoptosis under particular conditions (11,27), we went on to examine whether IB␣M might sensitize mesangial cells to apoptosis induced by other stimuli. An impressive body of data has implicated reactive oxygen species in the pathogenesis of glomerulonephritis (28), in activation of NF-B in some cell types (29), and in triggering apoptosis (30).…”