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. 2020 Sep 7;11:4435. doi: 10.1038/s41467-020-18288-w

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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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Fig. 6 — a Top panel: FISH for notch1 (green) and h3 (red) during steady state (stage 0) and during early stages of WBR. Bottom panel: FISH for notch2 (green) and h3 (red) during steady state (stage 0) and during early stages of WBR. Images are representatives of four independent experiments. Scale bar 20 μm. b Table showing the percentages of vessel fragments reaching stage 4 at day 14 post injury during treatment with different doses of inhibitors of canonical wnt signaling (Endo-IWR), Notch-signaling (DAPT) or control drugs Exo-IWR (1 μM) and the Notch-sparing gamma-secretase modulator E2012 (1 μM). The number of colonies that reached stage 4 was counted at 14 days post injury. Percentages represent the number of fragments reaching stage 4, with n = 14–18 fragments for each condition. Controls (subclones of the same genotype) received vehicle only. c FISH for pou3 (green) and h3 (red) showing a reduction in proliferating pou3+ cells 72 h after surgery when treated with an inhibitor of either Notch or Wnt signaling. Images are representatives of four independent experiments. Scale bars 20 μm.