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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Abnormal expression of long non-coding RNAs in myocardial infarction
Tao Wu1, Huan-Dong Wu2, Zao-Xian Xu2
1Hangzhou JunKangYiDe Hospital, No.26 North Xueyuan Road, Hangzhou, 310011, Zhejiang Province, People's Republic of China.
This study identified dysregulated long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) in myocardial infarction (MI) mouse models. These findings offer insights into the molecular mechanisms underlying MI pathogenesis.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Gene Expression Profiling
Background:
- Myocardial infarction (MI) remains a primary global cause of mortality.
- Understanding the molecular underpinnings of MI is crucial for developing effective treatments.
Purpose of the Study:
- To investigate dysregulated long non-coding RNAs (lncRNAs) in myocardial infarction (MI).
- To elucidate the underlying mechanisms of lncRNA involvement in MI pathogenesis.
Main Methods:
- Microarray analysis of lncRNA and mRNA expression in left ventricular tissues of MI and sham mice.
- Differential expression analysis, co-expression network construction, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
- Quantitative real-time polymerase chain reaction (qRT-PCR) for validation of differentially expressed lncRNAs.
Main Results:
- Identified 168 differentially expressed lncRNAs (DELs) and 126 differentially expressed mRNAs (DEMs) in MI.
- Constructed a co-expression network involving 219 nodes and 1775 edges.
- Validated specific lncRNAs (ENSMUST00000124047, AK166279, ENSMUST00000121611, NR_015515) with altered expression in MI.
Conclusions:
- The study identified a comprehensive profile of dysregulated lncRNAs and mRNAs in myocardial infarction.
- Enriched signaling pathways in MI include complement and coagulation cascades, and cytokine-cytokine receptor interactions.
- These findings contribute to understanding MI pathogenesis and may guide future therapeutic strategies.
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