Increased apoptosis and expression of FasL, Bax and caspase-3 in human lupus nephritis class II and IV

Abstract

Apoptosis is involved in glomerular injuries leading to glomerulonephritis. However, the role of renal cellular apoptosis in the pathogenesis and progression of human lupus nephritis (LN) is controversial, and studies on the expression of apoptosis-related proteins, such as FasL, Bax and caspase-3, in different classifications of human LN renal tissues are limited. Thirty-two samples of LN tissues, including 10 cases of class II and 22 cases of class IV LN, and 5 cases of human normal renal tissues were obtained. Expression of FasL, Bax and caspase-3 proteins in LN tissues was examined by immunohistochemical staining. Apoptotic cells were evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Expression of FasL, Bax and caspase-3 and TUNEL-positive cells in glomerular parenchymal cells, renal tubular epithelial cells and interstitial inflammatory cells were higher in LN tissues compared with controls. Expression of Bax and caspase-3, but not FasL, was significantly higher in glomeruli of class IV LN than those of class II LN. The apoptotic cell count per glomerulus was significantly higher in class IV LN than class II LN (p<0.05). Increased apoptosis and the expression of FasL, Bax and caspase-3 in human LN suggest that apoptosis might be induced through pathways of these proteins in the pathogenesis process and play an important role in LN progression through Bax and caspase-3, but not FasL.