Adriamycin increases podocyte permeability: evidence and molecular mechanism.
- Author:
Xiaozhong LI
1
;
Haitao YUAN
;
Xueguang ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Albumins; metabolism; Animals; Cadherins; analysis; Cell Membrane Permeability; drug effects; Cells, Cultured; Dexamethasone; pharmacology; Doxorubicin; pharmacology; Epithelial Cells; drug effects; Kidney Glomerulus; cytology; drug effects; Mice
- From: Chinese Medical Journal 2003;116(12):1831-1835
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the increased podocyte permeability by evidence of adriamycin (AD) and its molecular mechanism.
METHODSIn this study, we explored the direct effects of AD on cultured mouse podocytes and the potential protection effects of Dexamethasome (Dex).
RESULTSAfter 24-hour AD (5 x 10(-7) mol/L) treatment, albumin passage through podocyte monolayers was increased by 2.27-fold (P < 0.01). AD caused a 62% decrease in Zonula Occluden-1 (ZO-1) protein (P < 0.05), suggesting that AD might increase podocyte permeability by disrupting tight junctions. Dex (1 x 10(-6) mol/L), co-administered with AD, protected podocytes from AD-induced increased albumin passage. This may be linked with an increased P-cadherin protein level to 1.93 fold of control (P < 0.01).
CONCLUSIONSAD has a direct, detrimental effect on podocyte permeability, probably through disrupting tight junctions; Dex could protect against AD-induced high podocyte permeability by upregulating adherent protein P-cadherin.
