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. 2019 Feb 14;9:2059. doi: 10.1038/s41598-019-39515-5

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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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Mice lacking ATF6α or ATF6β protein have reduced hypertrophy after short-term pressure overload. (a) Gravimetric measurement of ventricle weight normalized to body weight (VW/BW) and (b) echocardiographic measurement of fractional shortening percentage (FS%) from Atf6^−/−, Atf6b^−/−, or control mice all also expressing the tTA transgene after 2 weeks of TAC or a sham surgery. (c) Gravimetric measurement of VW/BW and (d), echocardiographic measurement of FS% from Atf6^−/−, Atf6b^−/−, or control mice in a pure C57BL/6 background without the tTA transgene after 2 weeks of TAC or a sham surgery. For each experiment, number of mice analyzed is given within the graph. *P < 0.05 versus sham of same genotype; ^#P < 0.05 vs Wt TAC for TAC comparisons only (Newman-Keuls multiple comparisons test). (e) Immunoblots of ER stress-associated proteins from heart homogenates of Atf6^−/−, Atf6b^−/−, or control mice all also expressing tTA after 2 weeks of TAC.