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. 2021 May 1;21:221. doi: 10.1186/s12872-021-01998-4

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© The Author(s) 2021

Open AccessThis 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/. 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 in a credit line to the data.

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Fig. 6 — CXCL12 was a target of miR-182-5p. a The binding sites between miR-182-5p and CXCL12 3′UTR were analyzed by starbase. b, c The interaction between miR-182-5p and CXCL12 was verified by dual-luciferase reporter assay and biotin RNA pull-down assay. d The efficiency of miR-182-5p inhibitor was checked using qPCR. e, f The expression of CXCL12 in HUVECs with miR-182-5p overexpression or inhibition was detected using qPCR and western blot. g, h The expression of CXCL12 in ox-LDL-treated HUVECs was detected by qPCR and western blot. i, j The expression of CXCL12 in ox-LDL-treated HUVECs with the addition of ATV was detected by qPCR and western blot. **P < 0.01, ***P < 0.001