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. 2017 Sep 7;8(9):e3044. doi: 10.1038/cddis.2017.439

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 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/4.0/

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Effect of angiotensin (AII) on transcription of different RAS components. Treatment of rat-isolated nuclei with AII induced an increase in the expression of mRNA for AT2 (a), angiotensinogen (ANG; b), renin (c) and PRRs (d), which was inhibited by simultaneous treatment with the AT1 receptor antagonist losartan (los), indicating that these effects are mediated via nuclear AT1 receptors. In contrast, the levels of AT1 receptor mRNA did not change significantly after AII administration (e). The role of AT1 receptors in these effects was confirmed in isolated nuclei from AT1 and AT2 KO mice treated with AII (f and g). The effects of AII on brain-isolated nuclei were also observed in nuclei from the MES 23.5 dopaminergic neuron cell line (h). Data are mean±S.E.M. *P<0.05 compared to control, ^#P<0.05 compared to the group treated with AII. One-way analysis of variance and Holm–Sidak post hoc test (a–e) and Student’s t-test (f–h) (n=4–8)