Expression of bcl-2 and bax in glomerular disease.
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.
Department of Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan.
A
A
Yoshimura
S
S
Uda
K
K
Inui
T
T
Nemoto
Y
Y
Sugenoya
S
S
Sharif
N
N
Yokota
S
S
Watanabe
T
T
Ideura
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002478:Cells, Cultured; D005920:Glomerular Mesangium / Q000166:cytology / Q000378:metabolism; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D007674:Kidney Diseases / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D006133:Growth Substances; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein