Related Experiment Video
Updated: Aug 8, 2026
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Gamma interferon stimulates monocyte chemotactic protein (MCP-1) in human mesangial cells
G Grandaliano1, A J Valente, M M Rozek
1Department of Medicine, University of Texas Health Science Center at San Antonio 78284-7882.
Insights
Human mesangial cells release monocyte chemotactic protein (MCP-1), a key factor in glomerulonephritis. Inflammatory cytokines like interferon-gamma significantly increase MCP-1 release, driving monocyte recruitment to inflamed glomeruli.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Cell-mediated immunity and monocyte infiltration are hallmarks of glomerulonephritis.
- Monocyte influx correlates with glomerular hypercellularity and proteinuria.
- Glomerular mesangial cells act as effector cells in glomerular pathology.
Purpose of the Study:
- To characterize and study the regulation of monocyte chemotactic protein (MCP-1) released by cultured human mesangial cells.
- To investigate the role of inflammatory cytokines in MCP-1 secretion.
Main Methods:
- Cultured human mesangial cells were used.
- MCP-1 release was measured by radioimmunoassay.
- MCP-1 mRNA expression was analyzed.
- Specific antibodies were used to identify MCP-1 forms.
Main Results:
- Serum-deprived mesangial cells constitutively release chemotactic activity neutralized by anti-MCP-1 antibody.
- Interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 (IL-1) markedly stimulate MCP-1 release.
- Cytokine-induced MCP-1 release is partly dependent on de novo synthesis, as evidenced by increased MCP-1 mRNA expression.
- At least three different forms of MCP-1 were identified.
Conclusions:
- Human mesangial cells synthesize and release multiple forms of MCP-1.
- IFN-gamma and other cytokines regulate MCP-1 secretion.
- IFN-gamma and MCP-1 are likely crucial in recruiting and activating monocytes in inflamed glomeruli.
Abstract:
Cell-mediated immunity and monocyte infiltration is a prominent histologic feature of several different types of glomerulonephritis. Monocyte influx to the glomerulus correlates with glomerular hypercellularity and proteinuria. Glomerular mesangial cells, in addition to being targets for inflammatory stimuli, are also effector cells that actively participate in glomerular pathology. Mesangial cells release monocyte chemotactic protein (MCP-1). In the present article, we characterized and studied the regulation of MCP-1 released by cultured human mesangial cells. Serum-deprived mesangial cells constitutively release chemotactic activity that is neutralized by specific anti-MCP-1 antibody. An antibody to baboon MCP-1 recognized 16, 15, and 11 kd proteins from concentrated conditioned medium that were consistent with the presence of different forms of MCP-1. Gamma interferon (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 (IL-1) markedly stimulate the release of MCP-1 as measured by a specific and sensitive radioimmunoassay. The release of MCP-1 in response to these cytokines is at least partially dependent on de novo synthesis of the protein because all three cytokines markedly stimulate the expression of MCP-1 mRNA. These data demonstrate that human mesangial cells synthesize and release at least three different forms of MCP-1 and that IFN-gamma and other cytokines regulate the secretion of MCP-1. IFN-gamma and MCP-1 may play a major role in the recruitment and activation of monocytes to the inflamed glomerulus.
