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. 2019 Feb 4;10(2):100. doi: 10.1038/s41419-019-1375-x

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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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Fig. 3 — a Upper panel showed western blot analysis of phosphorylation of MAPK 42/44 under the treatment with thrombin 0.5 U/mL and lower panel showed under the treatment with APC 1.0 ng/mL. b Quantitative results of western blot analysis of the treatment with thrombin (upper panel) and APC (lower panel). Results are means ± SEM (n = 4). *p < 0.05 compared with the HUVECs under no treatment by Mann–Whitney U-tests. c Upper panel showed western blot analysis using β-arrestin-2 knockdown cells (miR βarrestin-2) or control cells (miR Cont) under no treatment or treatment with APC 1.0 ng/mL. Lower panel showed quantitative results of western blot analysis using β-arrestin-2 knockdown cells (miR β arrestin-2) (n = 4) compared with control cells (miR Cont) (n = 4) under treatment with APC. Results are means ± SEM (n = 4). Data were analyzed compared with multiple groups by Kruskal–Wallis tests. *p < 0.05 compared with control cells under treatment of APC