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. 2022 Oct 11:2022:8428596.
doi: 10.1155/2022/8428596. eCollection 2022.

Activation of PTEN/P13K/AKT Signaling Pathway by miRNA-124-3p-Loaded Nanoparticles to Regulate Oxidative Stress Attenuates Cardiomyocyte Regulation and Myocardial Injury

Yuan Cheng  1 , Qing He  1   2 , Na Li  1 , Mengdi Luo  1
Affiliations

Activation of PTEN/P13K/AKT Signaling Pathway by miRNA-124-3p-Loaded Nanoparticles to Regulate Oxidative Stress Attenuates Cardiomyocyte Regulation and Myocardial Injury

Yuan Cheng et al. Oxid Med Cell Longev. .

Retraction in

Abstract

As a common cardiovascular disease, acute myocardial infarction seriously affects the health and life of patients. miRNAs play an important role in acute myocardial infarction. Based on miRNA obtained from the previous sequencing, this study investigated whether miRNA (miR)-124-3p-loaded nanoparticles (NPs) affect the phenotype of the acute myocardial infarction (AMI) rat. Nano-miR-124-3p decreased the myocardial infarction area, improved the myocardial tissue structure, and increased the degree of fibrosis. Nano-miR-124-3p decreased apoptosis and the expression of cleaved caspase 3, indicating its role in protecting and repairing the myocardium. To further verify the action mechanism of miRNA, a potential target gene of miR-124-3p, PTEN was identified by STARBASE and further confirmed using double luciferase assays. Following cotransfection of nano-miR-124-3p and PTEN, the areas of tissue structure damage, myocardial infarction, and fibrosis were substantially elevated. The expression of cleaved caspase 3 and the apoptosis rate in the nano-miR-124-3p and PTEN cotransfection group was also significantly increased. Bioinformatics analysis revealed that miRNA-124-3 may regulate oxidative stress injury by targeting PTEN. Taken together, miR-124-3p could protect and repair myocardial tissues through targeting PTEN.

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Conflict of interest statement

The authors declare no competing interest.

Figures

Figure 1
Figure 1
Histological examination of rats with myocardial infarction. (a) Myocardial infarct size was determined by TTC staining. (b) HE staining. (c) Masson stainings. (d) TUNEL staining. (e) Western blot of cleaved caspase 3 expression.
Figure 2
Figure 2
Protection and restoration of myocardial tissue by nano-miR-124-3p. (a) qPCR detection of miR-124-3p expression. (b) TTC staining. (c) HE staining. (d) Masson staining. (e) TUNEL staining.
Figure 3
Figure 3
Prediction and detection of PTEN being a target gene of miR-124-3p. (a) Prediction results of PTEN for miR-124-3p via STARBASE database. (b) The relative luciferase activity illustration using double luciferase assay. PTEN expression in both model and Sham groups were detected by western blot (c) and qPCR (d), respectively. (e) Detection of PTEN, P-P13K, and P-AKT expression by western blot after overexpression and inhibition of miR-124-3p.
Figure 4
Figure 4
Protection and restoration effects of nano-miR-124-3p on damaged myocardial tissue via targeting PTEN. (a) TTC staining. (b) HE staining. (c) Masson staining. (d) TUNEL staining. (e) Detection of cleaved caspase 3 expression by western blot after overexpression of nano-miR-124-3p and coexpression of nano-miR-124-3p and PTEN.
Figure 5
Figure 5
miRNA-124-3p may regulate oxidative stress injury by targeting PTEN. (a) GO enrichment. (b) Venn. (c) PPI. (d) Chord diagram.
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