Related Experiment Videos
Bcl-2 expression and apoptosis in nephrotoxic nephritis
H Sugiyama1, N Kashihara, T Onbe
1Department of Medicine III, Okayama University Medical School, Japan.
Experimental Nephrology
|January 23, 1998
Summary
Overexpression of the Bcl-2 protein may worsen glomerulonephritis by prolonging glomerular cell survival. Apoptosis, or programmed cell death, appears crucial for resolving the later stages of nephrotoxic nephritis.
Area of Science:
- Nephrology
- Cell Biology
- Oncology
Background:
- The Bcl-2 proto-oncogene product inhibits apoptosis, promoting cell survival.
- Understanding apoptosis regulation is key in glomerulonephritis pathogenesis.
Purpose of the Study:
- To investigate Bcl-2 protein expression and apoptosis during rat nephrotoxic nephritis.
- To correlate Bcl-2 levels with cellular events in glomerulonephritis.
Main Methods:
- Immunohistochemistry for Bcl-2 protein and proliferating cell nuclear antigen.
- Light and electron microscopy for morphologic changes.
- In situ DNA nick end labeling for apoptosis detection.
Main Results:
- Bcl-2 expression and cell proliferation peaked at 24 hours in the heterologous phase.
- Glomerular hypercellularity and apoptosis peaked on day 14 in the autologous phase.
- Glomerulonephritis resolved following the autologous phase.
Conclusions:
- Bcl-2 overexpression may contribute to glomerular cell survival and glomerulonephritis exacerbation.
- Apoptosis appears to be an active mechanism in resolving the autologous phase of nephrotoxic nephritis.