Expression of Fas, Bcl‐2 and p53 molecules in glomerulonephritis and their correlations with clinical and laboratory findings*

Abstract

Apoptosis plays a crucial role in glomerulonephritis (GN) as a regulatory mechanism and is controlled by various molecules including Fas antigen, Bcl-2 and p53 oncoproteins. The aim of the present study is to evaluate the correlation between the expression of these molecules and clinical and laboratory data in different types of GN. The expression of Fas antigen, Bcl-2 and p53 protein in five normal human kidney specimens and 55 tissues from patients with several types of GN were examined by immunohistochemistry and correlated with clinical and laboratory findings. The number of Fas-positive intraglomerular cells was significantly increased in proliferative GN when compared with non-proliferative cases. Numbers of Bcl-2- and p53-positive cells in proliferative GN were not different from the non-proliferative cases and there was no correlation between the changes in Fas, Bcl-2 and p53 themselves. Significant correlation of expression of these molecules with clinical and laboratory findings was not found, except between p53 and blood urea nitrogen levels. Apoptosis is a complex molecular process and the results of the present study should be supported with other methods to understand whether apoptosis contributes to progression or resolution of GN. Increased glomerular expression of Fas, Bcl-2 and p53 molecules in all types of GN might contribute new therapeutic approaches by modulating the expression of these molecules.