beta-Catenin mediates adriamycin-induced albuminuria and podocyte injury in adult mouse kidneys.
Nephrol Dial Transplant
; 25(8): 2437-46, 2010 Aug.
Article
em En
| MEDLINE
| ID: mdl-20237062
BACKGROUND: Glomerular slit diaphragm (SD) represents a modified adherens junction composed of molecules belonging to both immunoglobulin and cadherin superfamilies. Cadherins associate with the cytosolic scaffolding protein beta-catenin, but the precise role of beta-catenin in mature or injured podocytes is not known. METHODS: The conditional podocyte-specific beta-catenin-deficient mouse line was generated using the doxycycline-inducible Cre-loxP system. Expression of the beta-catenin-deficient gene was turned off at the age of 8 weeks by doxycycline treatment and the kidney phenotype was analysed. In addition, beta-catenin-deficient and control mice were treated with adriamycin (ADR) and analysed for albuminuria and morphological alterations. RESULTS: Deletion of beta-catenin in mature podocytes did not change the morphology of podocytes nor did it lead to albuminuria. However, lack of beta-catenin attenuated albuminuria after ADR treatment. Electron microscopic examination showed increased podocyte foot process effacement associated with SD abnormalities in ADR-treated control mice compared to beta-catenin-deficient mice. CONCLUSIONS: These results show that beta-catenin in podocytes is dispensable for adult mice, but appears to be important in modulating the SD during ADR-induced perturbation of the filtration barrier.
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Base de dados:
MEDLINE
Assunto principal:
Doxorrubicina
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Albuminúria
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Beta Catenina
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Glomérulos Renais
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Antibióticos Antineoplásicos
Limite:
Animals
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article