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. 2021 Mar 3;21:121. doi: 10.1186/s12872-020-01742-4

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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. 4 — miR-130a-5p targets HMGB2. a TargetScan identified the binding site between miR-130a-5p and HMGB2 3′ untranslated region. b Dual-luciferase reporter gene assay verified the targeting relation between miR-130a-5p and HMGB2. c, d RT-qPCR and western blot analysis indicated that mRNA expression and protein level of HMGB2 in MIRI mice were both lowered by overexpressed miR-130a-5p, n = 4. The images of d shown are cropped. Two-way ANOVA was used to determine data in panel b and one-way ANOVA was employed to determine data in panels c, d. Tukey’s multiple comparisons test was applied for post hoc test. **p < 0.01; ^##p < 0.01. miR microRNA, HMGB high mobility group box, RT-qPCR reverse transcription quantitative polymerase chain reaction, MIRI myocardial ischemia reperfusion injury, ANOVA analysis of variance