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Published on: January 19, 2022
Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice
Jie Chen1,2,3, Jiahong Gong1,2, Haili Chen1,2
1Rehabilitation Medicine Center, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Insights
Stroke causes heart muscle atrophy and dysfunction by altering gene expression in the heart. This study reveals unique cardiac transcriptome changes following middle cerebral artery occlusion (MCAO) in mice.
Area of Science:
- Cardiology
- Neuroscience
- Molecular Biology
Background:
- Stroke can cause cardiac dysfunction even without primary heart disease.
- Mechanisms linking neurological deficits and cardiac issues post-stroke are unclear.
- Understanding this interaction is crucial for patient outcomes.
Purpose of the Study:
- Investigate stroke's effects on cardiac function.
- Identify cardiac transcriptome changes after stroke.
- Elucidate molecular mechanisms of stroke-induced cardiomyopathy.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in mice.
- Measurement of heart weight and cardiomyocyte size.
- RNA sequencing (RNA-seq) for transcriptome analysis.
- Quantitative PCR for gene expression validation.
Main Results:
- Stroke induced myocardial atrophy, evidenced by decreased heart weight/tibia length ratio and cardiomyocyte size.
- RNA-seq identified 383 differentially expressed genes (DEGs) in the myocardium.
- DEGs suggest suppressed immune response, altered collagen synthesis, and changes in enzyme activity.
- DEGs are located in cardiomyocyte membranes/extracellular regions, potentially mediating cardiac dysregulation.
Conclusions:
- Stroke triggers a distinct myocardial transcriptome response.
- This response leads to rapid cardiac atrophy and dysfunction.
- Findings highlight a direct link between neurological events and cardiac health.
Background:
Stroke can induce cardiac dysfunction in the absence of primary cardiac disease; however, the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart.
Results:
Stroke significantly decreased heart weight/tibia length ratio and cardiomyocyte cross-sectional areas and increased atrogin-1 and the E3 ubiquitin ligase MuRF-1, indicating myocardial atrophy in MCAO-induced mouse hearts. RNA sequencing of mRNA revealed 383 differentially expressed genes (DEGs) in MCAO myocardium, of which 221 were downregulated and 162 upregulated. Grouping of DEGs based on biological function and quantitative PCR validation indicated that suppressed immune response and collagen synthesis and altered activity of oxidoreductase, peptidase, and endopeptidase may be involved in MCAO-induced cardiomyopathy. The DEGs were mainly distributed in the membrane or extracellular region of cardiomyocytes and acted as potential mediators of stroke-induced cardiac dysregulation involved in cardiac atrophy.
Conclusion:
Stroke induced a unique transcriptome response in the myocardium and resulted in immediate cardiac atrophy and dysfunction.
