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. 2019 May 22;9:7679. doi: 10.1038/s41598-019-44194-3

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Attenuation of MYH9 depletion-induced actin cytoskeleton disruption and impaired filtration barrier by NAC. (A) Cultured podocytes grown on coverslips were fixed with 4% PFA and immunolabeled with FITC-phalloidin (green) and junctional marker ZO-1 (red). NAC-treated control or MYH9-depleted podocytes showed restored actin stress fibers and ZO-1 staining. Magnification 40x; bar = 50 μm. (B) Losartan and (C) NAC effect on podocyte permeability. Podocytes on the Transwell filter chamber were treated with Ang II in the presence of losartan or NAC. Then, 40 mg/ml BSA-containing medium was added into the lower chambers, and the upper chambers were sampled. The data are presented as the means ± SD, n = 3. The experiments were repeated twice. *P < 0.05 compared with siCTRL. ^#P < 0.05 compared with the siMYH9 control. ^†P < 0.05 compared with siMYH9 control podocytes treated with Ang II.