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Updated: Dec 16, 2025
Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart
Published on: February 3, 2023
RNA-sequencing-based transcriptome analysis of cantharidin-induced myocardial injury
Youyou Zhang1, Liang Liu1, Liang Ren1
1Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
The cardiotoxicity of cantharidin has been well characterized, but the understanding of the underlying mechanism(s) is incomplete. To more fully understand the differentially expressed genes (DEGs) in cantharidin-induced myocardial injury, Sprague-Dawley rats were exposed to cantharidin (1.34 mg/kg or 2.67 mg/kg) for 24 h and then the heart was sampled for pathologic changes analysis and RNA-sequencing-based transcriptomic profiling. In addition, serum troponin T (TN-T) levels were also tested using the enzyme-linked immunosorbent assay method. The results showed that cantharidin could cause myocardial damage and elevated serum TN-T levels. The genes with a fold change ≥2 were considered as DEGs and we found 38 DEGs that were mainly enriched in eight pathways revealed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The cellular component of gene ontology analysis showed that the DEGs were mostly enriched in the extracellular matrix. In conclusion, our present study demonstrated that cantharidin induces myocardial injury by multiple modulatory mechanisms, which provide new insights for further study of the pathophysiologic mechanism of cantharidin-induced myocardial injury.
Insights
Cantharidin exposure causes heart damage and elevated troponin T levels in rats. This study identified 38 differentially expressed genes, primarily linked to the extracellular matrix, offering new insights into cantharidin-induced myocardial injury mechanisms.
Area of Science:
- Toxicology
- Molecular Biology
- Cardiovascular Research
Background:
- The cardiotoxicity of cantharidin is known, but its precise molecular mechanisms remain unclear.
- Understanding gene expression changes is crucial for elucidating cantharidin-induced myocardial injury.
Purpose of the Study:
- To investigate the differentially expressed genes (DEGs) in rats exposed to cantharidin.
- To analyze the pathways and cellular components affected by cantharidin-induced myocardial injury.
Main Methods:
- Sprague-Dawley rats were administered cantharidin (1.34 mg/kg or 2.67 mg/kg) for 24 hours.
- Cardiac tissue underwent pathologic analysis and RNA-sequencing for transcriptomic profiling.
- Serum troponin T (TN-T) levels were measured using ELISA.
Main Results:
- Cantharidin induced significant myocardial damage and elevated serum TN-T levels.
- 38 DEGs (fold change ≥2) were identified.
- KEGG pathway analysis revealed enrichment in eight pathways, with Gene Ontology analysis highlighting the extracellular matrix as a key cellular component.
Conclusions:
- Cantharidin induces myocardial injury through multiple modulatory mechanisms.
- The identified DEGs and enriched pathways provide novel insights into the pathophysiology of cantharidin cardiotoxicity.
- Further research into these mechanisms is warranted for a comprehensive understanding.
