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. 2020 Aug 18;43(6):1161–1174. doi: 10.1007/s13402-020-00549-x

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — The PAR1-MMP9 axis reduces macrophage induced cytotoxicity. (A-B) MTT viability assay of PANC-1, MIA PaCa-2 and Capan-2 cells in RPMI-1640 (white) or M0-CM (blue) medium. Shown in the effect of PAR1 inhibition with 500 nM Vorapaxar (A) or MMP9 inhibition with 5 μM GM6001 (B). Decreased viability is calculated relative to the viability of control-treated cells. Shown is the mean ± SEM (n = 6); One-way ANOVA. (C) Annexin V-FITC+ cells in mock (RPMI-1640), M0-CM, or positive-control (Gemcitabine) treated PANC-1 and MIA PaCa-2 cells at t = 48 h. Left panel: gating strategy for the Annexin V+ population. The FITC gate was set on antibody controls. Right panel: geometric Mean Fluorescent Intensity (gMFI) on the FITC channel (Annexin V density) for Mock, M0-CM, and positive-control treated cells from the previous panel is given. Shown is the mean ± SEM (n = 3); One-way ANOVA