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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
Dysregulated expression of microRNAs and mRNAs in myocardial infarction
Yaping Wang1, Xiaohong Pan2, Youqi Fan2
1Department of Cardiology, Second Affiliated Hospital, College of Medicine, Zhejiang UniversityHangzhou 310009, PR China; Key Lab of Cardiovascular Disease, Second Affiliated Hospital, College of Medicine, Zhejiang UniversityHangzhou 310009, PR China.
Abstract:
Acute myocardial infarction (AMI) is a major cause of mortality in the general population. However, the molecular phenotypes and therapeutic targets of AMI patients remain unclear. By profiling genome-wide transcripts and microRNAs (miRNAs) in a cohort of 23 AMI patients and 23 non-AMI patients, we found 218 dysregulated genes identified in the infarcted heart tissues from AMI patients relative to non-AMI controls. Pathway enrichment analysis of the dysregulated genes pointed to cell signaling/communication, cell/organism defense and cell structure/motility. We next compared the expression profiles of potential regulating miRNAs, suggesting that dysregulation of a number of AMI-associated genes (e.g., IL12A, KIF1A, HIF1α and CDK13) may be attributed to the dysregulation of their respective regulating miRNAs. One potentially pathogenic miRNA-mRNA pair, miR-210-HIF1α, was confirmed in a mouse model of myocardial infarction (MI). Inhibition of miR-210 expression improved the survival and cardiac function of MI mice. In conclusion, we presented the pathologic relationships between miRNAs and their gene targets in AMI. Such deregulated microRNAs and mRNAs like miR-210 serve as novel therapeutic targets of AMI.
Insights
Researchers identified molecular differences in heart tissue from patients with acute myocardial infarction (AMI). They found that deregulated microRNAs (miRNAs) like miR-210 contribute to AMI, offering potential new therapeutic targets for heart attack treatment.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Acute myocardial infarction (AMI) is a leading cause of death globally.
- Understanding the molecular basis of AMI is crucial for identifying effective treatments.
- Current knowledge of molecular phenotypes and therapeutic targets in AMI patients is limited.
Purpose of the Study:
- To investigate genome-wide transcript and microRNA (miRNA) expression profiles in AMI patients.
- To identify dysregulated genes and their associated miRNAs in infarcted heart tissue.
- To explore novel therapeutic targets for AMI based on miRNA-gene interactions.
Main Methods:
- Genome-wide transcript and miRNA profiling of heart tissues from 23 AMI patients and 23 non-AMI controls.
- Pathway enrichment analysis to identify biological functions of dysregulated genes.
- Validation of a specific miRNA-mRNA interaction (miR-210-HIF1α) in a mouse model of myocardial infarction (MI).
Main Results:
- Identified 218 dysregulated genes in AMI heart tissues compared to controls.
- Dysregulated genes are involved in cell signaling, defense, and structure/motility.
- Confirmed a pathogenic role for miR-210 in MI, where its inhibition improved cardiac function and survival in mice.
Conclusions:
- Presented novel insights into the pathological relationships between miRNAs and their gene targets in AMI.
- Highlighted deregulated miRNAs and mRNAs, such as miR-210, as potential novel therapeutic targets for AMI.
- Demonstrated that targeting miR-210 can be a viable therapeutic strategy for myocardial infarction.
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