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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.
Abstract:
Myocardial infarction (MI) is the leading cause of fatality worldwide. Our study aimed to investigate the dysregulated long non-coding RNA (lncRNA) in MI and elucidate the mechanism of it in MI. The lncRNA and mRNA expression profiling of the whole left ventricular tissue of MI mice model (8 mice) and Sham group (8 mice) was obtained based on microarray analysis. Differentially expressed lnRNAs/mRNA (DELs/DEMs) were identified in MI. DELs/DEMs co-expression network construction, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted to predict the biological functions of DEMs. Quantitative real-time polymerase chain reaction (qRT-PCR) was subjected to validate the abnormally expressed DELs in left ventricular tissues of MI mice model. Total of 168 DELs (37 up- and 131 down-regulated) and 126 DEMs (87 up- and 39 down-regulated) were identified in MI compared with Sham group. The co-expression network of candidate DELs and DEMs was constructed, which covered 219 nodes and 1775 edges. The qRT-PCR validation results indicated that ENSMUST00000124047 was significantly down-regulated in MI group and AK166279 was significantly up-regulated in MI group. ENSMUST00000121611 and NR_015515 had the up-regulated tendency in MI group compared with Sham group. The DEMs in MI were significantly enriched in 41 signaling pathways including complement and coagulation cascades, cytokine-cytokine receptor interaction and chemokine signaling pathway. The expression profiling of dysregulated DELs in MI was identified. Our results might provide useful information for exploring the pathogenesis mechanism of MI.
Insights
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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