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. 2021 Jul 16;9:702890. doi: 10.3389/fcell.2021.702890

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Copyright © 2021 Wang, Zhang, Liu, Xu and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pro-inflammatory phenotype of damaged LSECs. After LSECs were treated with different stimuli [vehicle, lipopolysaccharide (LPS), monocrotaline (MCT), and MCT + LPS], the following parameters were examined: (A) the supernatant CXCL1 and TNF-α, tested by ELISA; (B) mRNA levels of CXCL1 and TNF-α; (C) phosphorylation of LSEC p65. (D) The influence of CXCL1 on neutrophil chemotaxis was evaluated by the number of trans-membrane migrated neutrophils in the Transwell experiment. (E) LSEC-derived CXCL1 was also examined by immunocytochemistry of CXCL1 (red) and RECA-1 (green, a marker of rat endothelial cells). (F) The co-localization of CXCL1 (red) and RECA-1 (green) was detected by immunohistochemistry in colitis-induced liver injury. Asterisk indicates that the level is significantly different from normal control. *p < 0.05; **p < 0.01; ***p < 0.001 by one-way ANOVA; n = 6 in each group; panels (A–C) are representative of three experiments; panel (C) is representative of one experiment, while other panels are representative of three experiments.