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Mesangial cell apoptosis: the major mechanism for resolution of glomerular hypercellularity in experimental mesangial
A J Baker1, A Mooney, J Hughes
1Department of Medicine, University Hospital, Nottingham, United Kingdom.
Abstract:
Increases in mesangial cell number may herald glomerular scarring, but they are not irreversible. This study sought mechanisms by which surplus glomerular mesangial cells can be cleared. A small proportion of cultured mesangial cells exhibited typical morphological features of apoptosis (programmed cell death), which was increased by growth factor deprivation or exposure to cycloheximide, stimuli known to increase apoptosis in other cell types. Apoptosis was confirmed by typical internucleosomal chromatin cleavage. In vivo, clear morphological evidence of mesangial apoptosis leading to phagocytosis by neighboring mesangial cells was obtained in self-limited mesangial proliferation induced in rats by Thy1.1 antibody, apoptosis occurring approximately 10-fold more frequently than in the healthy rat glomerulus. Indeed, changes in glomerular cell number in Thy1.1 nephritis strongly suggested that apoptosis is the major cell clearance mechanism counterbalancing cell division, thereby mediating resolution of glomerular hypercellularity in experimental mesangial proliferation.
Insights
Glomerular mesangial cell proliferation can be resolved through programmed cell death (apoptosis). This natural cell clearance mechanism, apoptosis, effectively reduces excess mesangial cells in kidney disease models.
Area of Science:
- Nephrology
- Cell Biology
- Pathology
Background:
- Mesangial cell proliferation can lead to glomerular scarring.
- Understanding mechanisms for resolving mesangial cell surplus is crucial for kidney health.
Purpose of the Study:
- To investigate the mechanisms responsible for clearing excess glomerular mesangial cells.
- To determine if apoptosis plays a role in resolving mesangial hypercellularity.
Main Methods:
- Cultured rat mesangial cells were treated with growth factor deprivation and cycloheximide.
- Apoptosis was assessed morphologically and by detecting internucleosomal chromatin cleavage.
- Mesangial apoptosis was evaluated in a rat model of Thy1.1 antibody-induced nephritis.
Main Results:
- Cultured mesangial cells demonstrated morphological features and chromatin cleavage indicative of apoptosis.
- Apoptosis occurred at a significantly higher rate (approximately 10-fold) in the glomeruli of rats with Thy1.1 nephritis compared to healthy controls.
- Evidence of mesangial apoptosis and subsequent phagocytosis by neighboring cells was observed in vivo.
Conclusions:
- Apoptosis is a key mechanism for clearing surplus glomerular mesangial cells.
- This programmed cell death pathway is vital for resolving glomerular hypercellularity and preventing scarring in experimental kidney injury.
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