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. 2024 Apr 8;14:8196. doi: 10.1038/s41598-024-58592-9

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Knockdown of RSAD2 in IFN-γ-stimulated human aortic smooth muscle cells results in reduced synthesis and secretion of CXCR3 ligands. Relative mRNA expression of (a) CXCL9 (n = 4), (b) CXCL10 (n = 3) and (c) CXCL11 (n = 3) in hAoSMCs transfected with RSAD2-targeting or scramble siRNAs and treated with IFN-γ for 44 h (normalized to the average of CTL KD). Protein quantification of (d) CXCL9 (n = 3), (e) CXCL10 (n = 3) and (f) CXCL11 (n = 3) in supernatant of hAoSMCs transfected with RSAD2-targeting or scramble siRNAs and stimulated with IFN-γ for 44 h. One-way ANOVA followed by Bonferroni’s multiple comparison test was employed to test for statistical significance. p value < 0.05 is considered statistically significant. CXCL9/10/11, CXC-motif ligand 9/10/11.