Expression of bcl-2 and bax in glomerular disease

Abstract

Bcl-2 may account in part for the maintenance of hypercellularity in human glomerular diseases through preventing cell death and by counteracting bax which may be expressed to regulate excessive proliferation. This process is associated with the effect of PDGF B-chain expression. Bax expression may be important in the cell loss leading to glomerulosclerosis and TGF-beta1 participates in this process by increasing bax expression. Thus, the balance of bcl-2/bax expression may be critical in the course of human glomerular diseases.

Renal bcl-2/bax expression in childhood Henoch–Schönlein nephritis: prognostic importance?

“…Proliferative glomerulonephritis shows increased mitotic activity in glomeruli or infiltrating inflammatory cells. Thus, recovery of the lesions probably depends on increased apoptotic removal of these cells (4,17). Our results support this theory.…”

“…Thus, the balance between them is critical for the progression of glomerular diseases. Bcl-2 expression correlates with proliferation/activation of mesangial cells (4,18,19). However, bax expression correlates with mesangial matrix expansion and type-IV collagen deposition.…”

“…However, bax expression correlates with mesangial matrix expansion and type-IV collagen deposition. Therefore, their relative expression is important in disease progression (4). Involvement of oxidative stress and reactive oxygen molecules (ROMs) in HSP is more indirect evidence for the role of apoptosis in HSN pathogenesis.…”

“…The best known and most extensively studied ones are antiapoptotic bcl-2 and proapoptotic bcl-2 associated X (bax), which block each other by heterodimerisation. Their relative expressions at cellular level determine the fate of involved cells, either in the direction of apoptosis or survival (2)(3)(4)(5).…”

Influence of glucosamine on glomerular mesangial cell turnover: implications for hyperglycemia and hexosamine pathway flux

“…Apoptosis is associated with an increase in levels of proapoptotic proteins such as Bax and decrease in the levels of prosurvival proteins like Bcl-2 (23,52,68). In line with these observations, we observed that glucosamine (10 mM) produced a significant increase in Bax levels that was accompanied by a concomitant decrease in Bcl-2 protein levels and occurred after the increase in p53 levels (Fig.…”