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. 2017 Aug 1;7:6970. doi: 10.1038/s41598-017-06718-7

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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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The overexpression of PRDX2 promote angiogenesis and myocardial hypertrophy. After 2 weeks of coronary artery ligation, serum from mice was harvested for RT-PCR analysis and myocardial tissue were harvested 4 weeks after artery ligation for immunohistochemical analysis. (A) Effects of PRDX2 on cell surface area of cardiomyocytes. (B) Cell surface area was calculated by measuring 10 random cardiomyocytes. (C–E) RT-PCR for ANP (C), PRDX2 (D) and VEGF (E) expression. The data are presented as means ± SD from three separate experiments from five to six mice in each group. *p < 0.05, ***p < 0.001 vs normal WT group. (F) The formation of microvascular cells in infarction region were stained with CD31. AB, aortic banding. The data are presented as means ± SD from 10 fields in each group. *p < 0.05, ***p < 0.001 vs normal WT group.