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. 2019 Jun 11;9:8481. doi: 10.1038/s41598-019-44834-8

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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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RAS possibly activates ER stress by inducing Yy1 expression: Yy1 (a transcription factor which regulates expression of ER stress markers) levels were significantly upregulated in Ang II treated cells compared to control group (A). Groups with RAS inhibitor telmisartan (A + T) and combination of telmisartan with P186 (A + B) showed significantly lower expression of Yy1 when compared to Ang II group. However, AT2 receptor blocker P-186 (A + P186) did not significantly reduce Yy1 expression (A). Interestingly, neither Ang II nor RAS antagonists changed the expression of TfII-i (B). Common letters indicate no significance. Data is presented as mean ± SEM (n = 3). p < 0.05.