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. 2017 Jun 12;7:3312. doi: 10.1038/s41598-017-03474-6

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© The Author(s) 2017

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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Vitamin D deficiency activates pulmonary RAS. (A) Immunofluorescence staining of the lung tissue with renin after two months of vitamin D deficiency. Original magnification: 200×. (B) Relative mRNA expressions of RAS components by real-time PCR. *P < 0.05, **P < 0.01, ***P < 0.001 Ctrl versus VDD group of the same age (n = 5–6 in each group). (C) Serum angiotensin II concentration in the mice after 2 months and six months of vitamin D deficiency. ***P < 0.001 Ctrl versus VDD group of the same age (n = 5–6 in each group). Agt: angiotensinogen; Ang: angiotensin; ACE1: angiotensin converting enzyme 1; AT1R: angiotensin type 1 receptor; Ctrl: control; VDD: chronic vitamin D deficiency; 2 m: 2 months; 6 m: 6 months. Statistics: Independent-sample two-tailed t-test.