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. 2016 Apr 7;7(4):e2183. doi: 10.1038/cddis.2016.89

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Copyright © 2016 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Autophagy inhibition by β-arrestins reduced podocyte viability by flow cytometric analysis. (a) Autophagy inhibition by gene silencing of ATG-3- or 3-methyladenine (3-MA)-induced apoptosis. (b) HG-induced apoptosis was alleviated by gene silencing of β-arrestins as well as by restoring defective autophagy with low dose of rapamycin. Overexpression of β-arrestins by pCMV6-β-arrestin-1 or pCMV6-β-arrestin-2 transfection in podocytes induced apoptosis, which could be attenuated by rapamycin. (means±S.E.M.; n=6; *P<0.05 versus control, †P<0.05 versus scramble of HG treatment, #P<0.05 versus overexpression of β-arrestins treatment)