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. 2019 May 20;9:7617. doi: 10.1038/s41598-019-44098-2

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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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FAK/Pyk2 inhibition blocks IL-1β-mediated pro-inflammatory adhesion molecule expression in HAoECs. (a) HAoECs were treated with DMSO, a dual FAK/Pyk2 inhibitor (PF-271, 2.5 μM) or a Src inhibitor (Dasatinib, 1 μM) for 1 h prior to IL-1β (20 ng/ml, 6 h) stimulation. Cropped images of immunoblotting for VCAM-1, ICAM-1, E-selectin, active FAK (pY397 FAK), FAK, active Src (pY418 Src), Src, and β-actin as loading control are shown. Full length blots shown in Supplemental Fig. 11. (b) HAoECs were treated with DMSO, a dual FAK/Pyk2 inhibitor (PF-271, 2.5 μM) or a FAK inhibitor (PF-228, 10 μM) for 1 h prior to IL-1β (20 ng/ml, 6 h) stimulation. Cropped images of immunoblotting for VCAM-1, ICAM-1, E-selectin, pY397 FAK, FAK, pY402 Pyk2, Pyk2, and β-actin as loading control are shown. Full length blots shown in Supplemental Fig. 12.