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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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Upregulation of MYH9 expression in TRPC6-depleted podocytes. (A) Validation of siRNA knockdown of Trpc6 (siTRPC6) in podocytes using Western blot. (B) Representative traces showing that Ang II-activated [Ca2⁺]_i was inhibited in TRPC6-depleted podocytes compared to control cells (siCTRL). (C) Summary of the results in panel B. (D) Representative traces showing that Ang II (1 μM, 1 h)-induced [Ca2⁺]_i increase was blunted by U73122, the active form of a PLCβ inhibitor, but not by its inactive analog (U73343, 2.5 μM, 1 h). (E) Summary of the results in panel E. (F) Western blot demonstrating the effects of siRNA knockdown of Trpc6 (siTRPC6) on MYH9 upregulation. (G) Schematic representation of the possible signaling pathway leading to podocyte injury by Ang II-mediated MYH9 downregulation. **P < 0.01.