Key result
RNA sequencing of mouse myocardial tissue 24 hours post-infarction identified 1367 differentially expressed genes and 42 differential alternative splicing genes, highlighting Fhl1, Fn1, and Postn as potential biomarkers.
Why the study?
Effective diagnostic biomarkers for acute myocardial infarction are lacking, and the relationship between alternative splicing and acute myocardial infarction remains unclear.
Differentially expressed genes and their alternative splicing, particularly Fhl1, Fn1, and Postn, show significant changes in a mouse model of AMI and may serve as potential biomarkers.
May identify novel AMI biomarkers via alternative splicing in mice; leaves open translation to clinical practice.
BACKGROUND: Acute myocardial infarction (AMI) is one of the leading causes of death in human being, and an effective diagnostic biomarker is still lacking. Whilst some gene association with AMI has been identified by RNA sequencing (RNA-seq), the relationship between alternative splicing and AMI is not clear. METHODS: We retrieved myocardial tissues within 24 h from mice with induced AMI and sham, and analysed the differentially expressed genes (DEGs) and differential alternative splicing genes (DASGs) by RNA-seq. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and protein interaction network analysis were performed on DEGs-DASGs-overlap genes. PCR was used to verify the expression levels of representative genes and alternative splicing in myocardial tissues of AMI and sham mice. RESULTS: 1367 DEGs were identified, including 242 up-regulated and 1125 down-regulated genes, among which there were 42 DASGs. GO analysis showed that the cellular component was primarily enriched in plasma membrane, cell membrane integrity and extracellular region. The molecular function was enriched in protein binding and metal ion binding. The biological process was primarily enriched in cell adhesion, immune system process and cell differentiation. KEGG analysis showed the enrichment was mainly in JAK-STAT and PI3K-AKT signalling pathway. Postn, Fhl1, and Fn1 were low-expressed while Postn alternative splicing was high-expressed in myocardial tissue of AMI mice, which was consistent with sequencing results. CONCLUSIONS: The pathogenesis of AMI involves differentially expressed genes and differential alternative splicing. These differentially expressed genes and their alternative splicing, especially, Fhl1, Fn1 and Postn may become new biomarkers of AMI.
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Liu et al. (2022) studied Acute myocardial infarction (n=22). Induced acute myocardial infarction (surgical ligation) vs. Sham operation was evaluated on Differentially expressed genes (DEGs) and differential alternative splicing genes (DASGs). RNA sequencing of mouse myocardial tissue 24 hours post-infarction identified 1367 differentially expressed genes and 42 differential alternative splicing genes, highlighting Fhl1, Fn1, and Postn as potential biomarkers.
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