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. 2019 Nov 26;8(23):e013112. doi: 10.1161/JAHA.119.013112

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© 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

PMC Copyright notice

Myocardial fibrosis following myocardial infarction (MI) was ameliorated in response to microRNA‐101 (miR‐101) elevation or runt‐related transcription factor 1 (RUNX1) depletion. The MI rats used for following assays were injected with lentiviral vectors expressing empty vector, miR‐101 mimic, miR‐101 inhibitor, and/or small interfering RNA targeting RUNX1 (si‐RUNX1). A, Representative images showing myocardial fibrosis in myocardial tissues of sham‐operated and MI rats assessed by Masson staining (×400). B, The percentage of myocardial fibrosis area in sham‐operated and MI rats. The data were expressed as mean±SD and analyzed using ANOVA (n=20 in each group). *P<0.05 compared with the sham‐operated rats. ^# P<0.05 compared with the MI rats injected with empty vector. ^& P<0.05 compared with the MI rats injected with both miR‐101 inhibitor and si‐RUNX1. NC indicates negative control.