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Expression of bcl-2 oncoprotein in various types of glomerulonephritis and renal allografts
L Nakopoulou1, K Stefananki, J Papadakis
1Department of Pathology, Medical School, University of Athens, Greece.
Background:
Bcl-2 oncogene was identified as a transcript associated with the t (14;18) and exhibits the unique functional role of blocking apoptosis. Apoptosis as a remodelling mechanism has been reported to embryonic and adult kidney. The aim of this study was to investigate the expression of bcl-2 protein in normal and diseased renal tissue and to define any correlation with the type of renal injury.
Materials And Methods:
Our material comprised of 10 normal adult kidneys, 31 renal allografts with acute (22) and chronic (9) rejection, and 70 renal biopsies with various types of primary (49) (31 proliferative and 18 non-proliferative) and secondary (21) glomerulonephritis. The immunohistochemical strept.ABC method was performed on paraffin sections for the detection of bcl-2 protein with a monoclonal antibody after microwave pretreatment.
Results:
Bcl-2 protein was detected in all the cases of normal and diseased renal tissue, showing an analogous expression. The antigen was expressed in a few parietal epithelial cells, and in the majority of distal and collecting tubular epithelial cells, but not in the glomerular capillary tuft. No difference was found in bcl-2 expression between cases of proliferative and non-proliferative glomerulonephritis as a whole, or between primary and secondary glomerulonephritis. Bcl-2 expression in acute and chronic rejection demonstrated a similar cytoarchitectural expression to the one observed in normal kidneys and glomerulonephritis. Bcl-2 was detected in podocytes near intraglomerular fibrotic lesions and in epithelial cells of early adhesions and cellular crescents, wherever observed in cases of glomerulonephritis. However, bcl-2 expression in proximal tubular epithelial cells was significantly higher in cases of proliferative glomerulonephritis than in non-proliferative glomerulonephritis (P<0.01), while bcl-2 expression in parietal epithelial cells in cases of chronic rejection was higher than in cases of acute rejection (P<0.08).
Conclusions:
The absence of bcl-2 expression in normal and diseased glomeruli suggests and supports the reported notion that the mechanism of apoptosis may be available in the injured glomerulus. Moreover, bcl-2 expression in podocytes near intraglomerular fibrotic lesions and in epithelial cells of early adhesions and cellular crescents indicates the deregulation of apoptosis and its possible role in the progression of glomerular scarring. Key words: apoptosis; bcl-2 oncoprotein; glomerulonephritis; immunohistochemical; renal rejection.
Insights
Bcl-2 protein is present in normal and diseased kidneys, but its absence in glomeruli suggests apoptosis is active there. Bcl-2 expression changes in certain kidney injuries may indicate its role in disease progression.
Area of Science:
- Nephrology
- Oncology
- Cell Biology
Background:
- The Bcl-2 oncogene inhibits apoptosis, a programmed cell death mechanism crucial for kidney development and maintenance.
- Understanding Bcl-2 expression in renal tissue is vital for comprehending kidney injury and disease.
Purpose of the Study:
- To investigate the expression of Bcl-2 protein in normal and diseased renal tissues.
- To correlate Bcl-2 expression patterns with different types of renal injury, including glomerulonephritis and rejection.
Main Methods:
- Utilized immunohistochemical methods on paraffin-embedded renal tissue sections.
- Detected Bcl-2 protein expression using a monoclonal antibody in normal kidneys, renal allografts (acute and chronic rejection), and biopsies with glomerulonephritis.
Main Results:
- Bcl-2 protein was detected in normal and diseased renal tissues, with analogous expression patterns.
- Expression was observed in parietal epithelial cells, distal and collecting tubular cells, but not in glomerular capillary tufts.
- Proximal tubular Bcl-2 expression was significantly higher in proliferative glomerulonephritis (P<0.01), and parietal epithelial cell expression was higher in chronic rejection (P<0.08).
Conclusions:
- Absence of Bcl-2 in glomeruli suggests apoptosis is active in injured glomeruli.
- Bcl-2 expression in podocytes and epithelial cells near fibrotic lesions and crescents indicates apoptosis deregulation and a potential role in glomerular scarring.