期刊
NEPHROLOGY DIALYSIS TRANSPLANTATION
卷 25, 期 8, 页码 2437-2446出版社
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfq076
关键词
albuminuria; beta-catenin; inducible mouse models; slit diaphragm
资金
- Einar and Karin Stroems Foundation
- Finnish Kidney Foundation
- Alfred Kordelin Foundation
- Orion Pharma Foundation
- Jalmari and Rauha Ahokas Foundation
- Paavo Nurmi Foundation
- Finnish Cultural Foundation
- Paulo Foundation
- Jenny and Antti Wihuri Foundation
- Maud Kuistila Memorial Foundation
- European Union [ADDNET LSFIB-CT-2003-503364, DiaNa LSHB-CT-2006-037681]
- Sigrid Juselius Foundation
- Finnish Diabetes Foundation
- Academy of Finland
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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