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Published on: October 31, 2017
Conditioned medium from alternatively activated macrophages induce mesangial cell apoptosis via the effect of Fas
Yuan Huang1, Fangjun Luo, Hui Li
1Department of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Abstract:
During inflammation in the glomerulus, the proliferation of myofiroblast-like mesangial cells is commonly associated with the pathological process. Macrophages play an important role in regulating the growth of resident mesangial cells in the glomeruli. Alternatively activated macrophage (M2 macrophage) is a subset of macrophages induced by IL-13/IL-4, which is shown to play a repair role in glomerulonephritis. Prompted by studies of development, we performed bone marrow derived macrophage and rat mesangial cell co-culture study. Conditioned medium from IL-4 primed M2 macrophages induced rat mesangial cell apoptosis. The pro-apoptotic effect of M2 macrophages was demonstrated by condensed nuclei stained with Hoechst 33258, increased apoptosis rates by flow cytometry analysis and enhanced caspase-3 activation by western blot. Fas protein was up-regulated in rat mesangial cells, and its neutralizing antibody ZB4 partly inhibited M2 macrophage-induced apoptosis. The up-regulated arginase-1 expression in M2 macrophage also contributed to this apoptotic effect. These results indicated that the process of apoptosis triggered by conditioned medium from M2 macrophages, at least is partly conducted through Fas in rat mesangial cells. Our findings provide compelling evidence that M2 macrophages control the growth of mesangial cells in renal inflammatory conditions.
Insights
Alternatively activated macrophages (M2 macrophages) induce apoptosis in rat mesangial cells via the Fas pathway. This finding highlights M2 macrophages
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Mesangial cell proliferation is a hallmark of glomerular inflammation in kidney diseases.
- Macrophages, particularly alternatively activated M2 macrophages, are implicated in regulating mesangial cell growth and repair in glomerulonephritis.
Purpose of the Study:
- To investigate the role of M2 macrophages in inducing apoptosis of rat mesangial cells.
- To elucidate the molecular mechanisms underlying M2 macrophage-mediated mesangial cell apoptosis.
Main Methods:
- Co-culture of bone marrow-derived M2 macrophages and rat mesangial cells.
- Analysis of mesangial cell apoptosis using Hoechst 33258 staining, flow cytometry, and Western blot for caspase-3 activation.
- Investigation of the role of Fas protein and arginase-1 in the apoptotic process.
Main Results:
- Conditioned medium from IL-4 primed M2 macrophages induced significant apoptosis in rat mesangial cells.
- Apoptosis was characterized by nuclear condensation, increased apoptotic rates, and enhanced caspase-3 activation.
- Fas protein upregulation and arginase-1 expression in M2 macrophages contributed to the pro-apoptotic effect.
Conclusions:
- M2 macrophages induce apoptosis in rat mesangial cells, partly through the Fas signaling pathway.
- Arginase-1 expression in M2 macrophages also plays a role in this apoptotic process.
- These findings demonstrate that M2 macrophages can regulate mesangial cell proliferation in renal inflammatory conditions.
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