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. 2020 Jul 28;10:12620. doi: 10.1038/s41598-020-69610-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 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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ER stress caused impaired efferocytosis in J774 cells in a ROCK/RhoA activation-dependent manner. (a) The induction of RhoA/Rho-kinase by TM (an antibiotic that promotes ER stress by blocking N-linked protein glycosylation) in J774 cells was evaluated using a ROCK activity assay kit. Six hours of stimulation with 1 or 10 μg/ml TM caused ROCK activation in a dose-dependent manner. The means were analyzed using an ANOVA; when the ANOVA indicated significance, Dunnett’s test was used to compare the groups with an internal control (n = 3) (*p < 0.05). (b) Y27632 (10 μM; a ROCK inhibitor) completely reversed the 10 μg/ml TM-induced impairment of efferocytosis (control mean PI, 19.7 ± 11.6). The mean PI is shown as a percentage of the control ± SEM of four replicates per group. The means were analyzed using an ANOVA, and when the ANOVA indicated significance, Tukey’s test was used to compare two conditions (*p < 0.05, **p < 0.01).