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Knockdown of miR-192 and miR-432 in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction

ABSTRACT: Knockdown of miR-192 and miR-432 in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction

PROVIDER: PRJNA805106 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17970500_1.fastq.gz	Fastqsanger.gz
	SRR17970500_2.fastq.gz	Fastqsanger.gz
	SRR17970501_1.fastq.gz	Fastqsanger.gz
	SRR17970501_2.fastq.gz	Fastqsanger.gz
	SRR17970502_1.fastq.gz	Fastqsanger.gz

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Project description:MicroRNAs (miRNAs) are a class of highly conserved endogenous noncoding single-stranded small RNAs with a length of 18-22 nucleotides. They are involved in regulation at the posttranscriptional and translational levels through the degradation and translation inhibition of messenger RNA (mRNA). It is estimated that at least 60% of all mammalian genes may be regulated by miRNAs. MiRNAs can help uncover the mechanisms of diseases and provide new entry points into therapy. Accumulated evidence has revealed that miRNAs are involved in the pathological process of cardiovascular disease through specific signaling pathways. To investigate the potential miRNAs for myocardial fibrosis post myocardial infarction, rat models of acute myocardial infarction (AMI) were established by ligating the anterior descending branch of the left coronary artery, while sham-operated rats were only threaded without ligation as a control group. There were three rats in each group. Thirteen differentially expressed miRNAs between the two groups were screened and their expression levels in the model group were all higher than those in the control group. The expression of miR-199a-5p was significantly increased in the model group in qRT-PCR, which was consistent with the results of the gene chip. KEGG enrichment analysis showed that the target genes of miR-199a-5p were enriched in the insulin signaling pathway. Furthermore, dual-luciferase reporter assay indicated that miR-199a-5p could negatively regulate the expression of GSK-3β. After transfection, the expression of miR-199a-5p was increased in the miR-199a-5p mimics group. The protein expression of GSK-3β was decreased in CFs transfected with miR-199a-5p mimics. In summary, our study identified miR-199a-5p could promote the progression of myocardial fibrosis after myocardial infarction by targeting GSK-3β, which provides novel targets for diagnosis and treatment of MF. In summary, our research suggests that miR-199a-5p promotes the progression of myocardial fibrosis after myocardial infarction through the activation of the insulin-PI3K/Akt-GSK-3β signaling pathway.

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Knockdown of miR-192 and miR-432 in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction

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