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. 2023 Sep 8;47(3):655–669. doi: 10.1007/s40618-023-02184-3

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© The Author(s) 2023

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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Fig. 6 — A miR-133a-3p seed match in 3’UTR of IGF-IR mRNA in humans and mice. Created with BioRender.com, B miR-133a-3p expression in C2C12 treated with HC alone and in combination with Rel expressed as a percentage compared to control. HC increased the levels of miR-133a-3p by about 235% compared to control (*p = 0.035); the use of Rel blocked the effect of HC (*p = 0.023, HC vs HC + Rel). C IGF-IR and PI3K/AKT/mTOR components protein expression in C2C12 transfected with miR-133a-3p inhibitor and treated with HC. Inhibition of miR-133a-3p induced IGF-IR protein up-regulation in both C2C12 cells. IGF-IR protein, instead, was down-regulated in presence of HC and transfection buffer. Conversely, IGF-IR protein was up-regulated in presence of both miR-133a-3p inhibitor and HC. D The blocking of miR-133a-3p induced a strong IGF-IR cytoplasmic and nuclear staining, compared to the control which showed a weaker cytoplasmic localization and poorer nuclear localization. HC treatment reduced IGF-IR protein staining compared to the control. In the presence of miR-133a-3p inhibitor, HC could no longer able to mediate its inhibitor effect on IGF-IR protein expression, restoring IGF-IR cytoplasmic and nuclear protein expression localization. HC hydrocortisone. Rel relacorilant