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. 2020 Jul 9;10:11404. doi: 10.1038/s41598-020-68223-8

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© The Author(s) 2020

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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Cilengitide reduces the profibrotic activation of cardiac PW1⁺ cells. (A) Representative cardiac sections (in the infarct zone) from vehicle- and cilengitide-treated mouse hearts immunostained with αSMA (green), β-gal (red), and DAPI (blue). White arrows indicate β-gal single-positive cells. (B) Quantification of αSMA⁺ cells within the total number of cells per field in vehicle- and cilengitide-treated post-MI hearts. (C) Quantification of β-gal⁺αSMA⁺ cells within the total number of cells per field in vehicle- and cilengitide-treated post-MI hearts. (D) Quantification of β-gal⁺ cells within the αSMA-negative cells in vehicle- and cilengitide-treated post-MI heart sections. (E) Representative cardiac sections (in the border zone) from vehicle- and cilengitide-treated mouse hearts immunostained with αSMA (green), CD31 (red), and DAPI (blue). (F) Quantification of CD31⁺αSMA⁺ vessels in the border zone in vehicle- and cilengitide-treated post-MI hearts. N = 18 fields at least from two animals per groups, *P < 0.05, **P < 0.01 and ***P < 0.001. Data are mean ± SD.