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. 2019 Jul 22;17:81. doi: 10.1186/s12964-019-0396-5

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — MIP1γ/CCR1 axis in retina endothelial cells contributed to the ameliorative effect of TNTL on endothelial dysfunction. a. showed that CCR1 downstream signalings in RECs cultured with SN from TNTL-treated BMDMs were blunted; b. showed that transcription of migration/invasion-associated genes was not activated in RECs cultured with SN from TNTL-treated BMDMs; c. showed that MIP1γ-induced RECs migration was blocked by the presence of CCR1 antagonist J-113863 (100 nM); d. showed that MIP1γ-induced loss of RECs monolayer integrity was blocked by the presence of CCR1 antagonist J-113863 (100 nM); e. showed MIP1γ-induced FITC-Dextran leakage through RECs monolayer was blocked by the presence of CCR1 antagonist J-113863 (100 nM). *p < 0.05, **p < 0.01, ***p < 0.001 when compared with model group