MiR-101a attenuates myocardial cell apoptosis in rats with acute myocardial infarction via targeting TGF-β/JNK signaling pathway
Authors: Y Fang
F-Y Liu
F-Q Zhou
X-F Zhao
S-S Wang
H-L Hu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-101a; myocardial cell apoptosis; acute myocardial infarction; regulatory mechanism; Sprague-Dawley rats
Affiliations: Department of Cardiology, Gaotang County People's Hospital of Shandong, Liaocheng, China. .

Abstract:  Objective: To investigate the effect of micro ribonucleic acid (miR)-101a on myocardial cell apoptosis in the rat model of acute myocardial infarction (AMI) and its regulatory mechanism. Materials and methods: A total of 30 Sprague-Dawley (SD) rats were randomly divided into the Sham group, Model group, and miR-101a mimic group, with 10 rats in each group. The rat model of AMI was established by the ligation of the anterior descending coronary artery. The rat left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were detected using a color Doppler ultrasonic apparatus. Subsequently, the miRNA online database (TargetScan) was adopted to predict miRNAs that could be able to regulate TGF-β1. Hematoxylin and eosin (H&amp;E) staining was conducted to reveal the histopathological morphology changes in the rat heart. The serum levels of cysteinyl aspartate specific proteinase-3 (Caspase-3) and Bcl-2-associated X protein (Bax) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the expression levels of the transforming growth factor-beta l (TGF-β1) and c-Jun N-terminal kinase (JNK) in rat heart were measured via Western blotting. Results: Through searching miRNA database, miR-101a and TGF-β1 messenger RNAs (mRNAs) had binding sites in the 3' untranslated region (3'UTR). Compared with those in Sham group, the rat LVEDV and LVESV were notably elevated, the histopathological morphology of the heart was seriously damaged, the apoptotic rate of myocardial cells and the levels of TGF-β1 and JNK proteins significantly increased in the Model group. Additionally, compared with those in the Model group, the LVEDV and LVESV of rats in miR-101a mimic group were significantly reduced, the histopathological morphology of the heart was markedly improved, and the apoptotic rate and the levels of TGF-β1 and JNK in rat heart were remarkably decreased. Conclusions: The myocardial cell apoptosis in AMI rats can be suppressed by overexpression of miR-101a by inhibiting the TGF-β1/JNK signaling pathway. 

Retracted: Yes

PubPeer comments:
 Int J Oncol 53: [Related article:] 1069-1082, 2018; DOI: 10.3892 ijo.2018.4482 Following the publication of this article, the authors have realized that the name of the second author was misspelt: u201cMinghai Dongu201d should have appeared as u201cMinhai Dongu201d. The correct information for the authors on this paper is presented above. The authors regret that this error made it into print, and apologize to the readership for any inconvenience caused. , 
 If one were to look closely, one may see small sliver overlaps in at least two sets of images in Figure 7. *** ![file] , 
 Corrected [10 January 2022] .  Subsequently to the publication of the above article and a Corrigendum that addressed the issue of a misspelling of one of the authors names (DOI: 10.3892 ijo.2019.4769; published online on April 2, 2019), the authors have subsequently discovered that Fig. 7 on p. 1079 contained a duplication in two of the panels that might cause the readers some confusion. The authors were able to re-examine the original data, repeat the experiment, and have decided to revise Fig. 7. The corrected version of Fig. 7, showing replacement data for the p-Akt and Cyclin D1 experiments, is shown on the next page. The authors confirm that these data continue to support the main conclusions presented in their paper, and are grateful to the Editor of *International Journal of Oncology* for allowing them this opportunity to publish a Corrigendum. They also apologize to the readership for any inconvenience caused.  ,