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. 2017 Apr 6;7:692. doi: 10.1038/s41598-017-00781-w

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© The Author(s) 2017

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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TME5 increases phosphorylation of signal-regulated kinase and level of Bcl-2 in ECs via GPR15. (a) Murine ECs from WT or GPR15 KO mice were treated with PBS or TME5 (250 ng/ml) for 48 hrs. In addition, GPR15 KO ECs were transduced with GPR15 expressing lentivirus vector followed by treatment with PBS or TME5 (250 ng/ml). (b) HUVECs, transfected with control siRNA or GPR15-specific siRNA, were treated with PBS or TME5 (250 ng/ml) for 48 hrs. For forced expression of GPR15, HUVECs were co-transfected with a GPR15-expression vector. Total proteins extracted from cells were analyzed by western blot. The PVDF membranes were probed with the indicated antibodies in sequence. Figure represents one from three independent experiments. Relative intensities of phospho-ERK, MCL-1 and BCL were analyzed in murine ECs (c) and HUVEC (d) (n = 3 in each). Data are shown as mean ± SD, and are compared using one-way ANOVA test. *p < 0.05; N.S., no significance.