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. 2023 Feb 6;13:2128. doi: 10.1038/s41598-023-29188-6

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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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Osa-miR172d-5p suppressed Tab1 upregulation in a bleomycin-induced fibrosis model. (A, B) C57BL male mice were treated with bleomycin (1 mg/kg bw intratracheal administration); after 1 week, the bleomycin-treated mice were treated with the negative control miR (3 nmol/mouse 5 times in 2 weeks, intraperitoneal injection with AteloGene) or miR Osa-miR172d-5p mimic miR (3 nmol/mouse five times in 2 weeks, intraperitoneal injection with AteloGene). After 3 weeks, the mice were sacrificed, their lung tissues were harvested, and fibrosis was assessed through the immunofluorescence analysis of Tab1 in mouse lungs (n = 5, 5, 4). (C) Correlation was performed via Spearman’s rank test (n = 14). Data are shown as mean ± SEM. **P < 0.01. ***P < 0.001 vs. control group.