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Published on: August 16, 2019
[Myocardial expression of Spry1 and MAPK proteins of viral myocarditis]
Hong-Fei Xu1, Lin Meng, Jian Yao
1Department of Forensic Medicine, School of Biology and Basic Medical Sciences, Medical College of Soochow University, Suzhou 215123, China. whhongfei@sina.com
Objective:
To discuss the myocardial expression of Spry1 and MAPK proteins of viral myocarditis (VMC), to reveal its mechanism of sudden death, and to provide guides for forensic identification of sudden cardiac death.
Methods:
Thirty Balb/c male mice were randomly divided into VMC group and control group, inoculated intraperitoneally with Coxsackievirus B3 and Eagel's solution, respectively. After the mice were sacrificed, the cardiac tissues of the mice were taken to proceed regular pathological examination. The changes of Spry1 protein, Spry1 mRNA and MAPK protein were detected by immunohistochemistry, Western blotting and real-time PCR.
Results:
Under light microscope, the pathologic changes included myocardial interstitial edema, inflammatory cells infiltration, myocardial necrosis, and focal and patchy necrosis of myocardial fiber in VMC group. The expression of Spry1 protein in VMC group was lower than that in control group (P < 0.05). There was slightly decreased expression of Spry1 of the mRNA level in VMC group (P > 0.05). But the MAPK protein expression in VMC group was higher than that in control group (P < 0.05).
Conclusion:
The pathway of MAPK/ERK involving Spry1 protein accelerates the expression of collagen, which may contribute to arrhythmia, heart failure and even sudden cardiac death.
Insights
Viral myocarditis (VMC) reduces Spry1 protein expression while increasing MAPK protein, potentially leading to sudden cardiac death. This finding aids in forensic identification of VMC-related fatalities.
Area of Science:
- Cardiovascular Pathology
- Molecular Biology
- Forensic Science
Context:
- Viral myocarditis (VMC) is a significant cause of sudden cardiac death.
- Understanding the molecular mechanisms underlying VMC-induced cardiac dysfunction is crucial.
Purpose:
- To investigate the myocardial expression of Spry1 and MAPK proteins in VMC.
- To elucidate the mechanism of sudden death in VMC.
- To provide insights for forensic identification of sudden cardiac death.
Summary:
- In a mouse model of VMC, significant pathological changes were observed, including myocardial necrosis.
- Spry1 protein expression was significantly decreased, while MAPK protein expression was significantly increased in VMC mice compared to controls.
- Spry1 mRNA levels showed a slight decrease, suggesting post-transcriptional regulation.
Impact:
- The MAPK/ERK pathway, influenced by Spry1, may accelerate collagen expression, contributing to arrhythmias, heart failure, and sudden cardiac death.
- These findings offer potential biomarkers for diagnosing VMC and identifying its role in sudden cardiac death cases.
- This research provides a foundation for developing targeted therapies for VMC.
Related Concept Videos
Myocarditis I: Introduction
Myocarditis II: Clinical Features and Diagnostic Tests
Myocarditis III: Medical Management
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy

