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. 2016 May 13;48(5):e233. doi: 10.1038/emm.2016.28

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Copyright © 2016 KSBMB.

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 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-nc-nd/4.0/

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The localization of glucocorticoid-induced transcript 1 (GLCCI1), podocyte-specific markers and proteins associated with the phosphoinositide 3-kinase (PI3K) signaling pathway in the rat glomerulus. (a) Staining of rat kidney sections with an antibody against GLCCI1 (red) is shown. The diabetic group showed low reactivity. However, GLCCI1 was regulated by wortmannin treatment. (b–d) The podocyte-specific proteins nephrin (green), podocin (red) and synaptopodin (green) showed a reactivity pattern similar to GLCCI1 following wortmannin treatment. (e) Serum/glucocorticoid-regulated kinase 1 (SGK1; red) was observed only in the diabetic group. We confirmed that SGK1 expression was decreased by wortmannin. (f) Forkhead box O3 (FOXO3A; red) was observed in the control group. The lower reactivity of FOXO3A was accompanied by the overexpression of SGK1 in the diabetic group. The localization of FOXO3A was regulated by wortmannin treatment. Original magnification: × 400. Scale bar, 50 μm.