Related Experiment Video
Updated: Aug 6, 2026
Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice
Published on: May 4, 2015
Induction of myocardial nitric oxide synthase by Coxsackie B3 virus in mice
N M Robinson1, H Y Zhang, A L Bevan
1King's College Hospital Medical School, London, UK. nick1robinson@compuserve.com
Background:
Inducible nitric oxide synthase (iNOS) expression is regulated by cytokines. This study investigated whether Coxsackie group B virus (CVB) myocarditis resulted in an environment suitable for induction of NOS in the murine heart.
Materials And Methods:
Myocardium was removed from mice infected with CVB3 and from controls. Histology, reverse transcriptase polymerase reaction (RT-PCR) for murine iNOS, NOS enzyme activity and immunohistochemistry were assessed.
Results:
Histology revealed severe myocarditis 7 days after infection with CVB3 but not in controls. RT-PCR using primers for murine iNOS detected iNOS mRNA in infected mice but not in controls. Calcium-independent NOS activity increased by day 5 after infection with a peak at day 7. Calcium-dependent NOS activity was present throughout, with a trend to lower levels during peak calcium-independent activity. Immunohistochemistry revealed iNOS to be localized to inflammatory cells rather than to myocytes.
Conclusion:
This study demonstrates the development of calcium-independent NOS activity and de novo gene transcription for iNOS in the murine myocardium in response to CVB3 infection. The nitric oxide produced at such high output may act at times as part of the immune defence as an antiviral agent and may be toxic to host tissue.
Insights
Coxsackie B virus infection induces nitric oxide synthase (NOS) in mouse hearts, leading to inflammation and potential tissue damage. This antiviral response may also harm host tissues.
Area of Science:
- Cardiovascular Research
- Virology
- Immunology
Background:
- Cytokines regulate inducible nitric oxide synthase (iNOS) expression.
- Coxsackie group B virus (CVB) infection can cause myocarditis.
- The role of iNOS in CVB-induced myocarditis is not fully understood.
Purpose of the Study:
- To investigate iNOS induction in murine hearts following CVB3 infection.
- To determine if CVB myocarditis creates a suitable environment for NOS induction.
Main Methods:
- Histological examination of infected murine myocardium.
- Reverse transcriptase polymerase reaction (RT-PCR) for murine iNOS mRNA.
- Measurement of NOS enzyme activity and immunohistochemistry.
Main Results:
- CVB3 infection caused severe myocarditis and detected iNOS mRNA in infected mice.
- Calcium-independent NOS activity increased significantly post-infection.
- iNOS was localized to inflammatory cells, not myocytes.
Conclusions:
- CVB3 infection induces de novo gene transcription and calcium-independent NOS activity in the murine heart.
- Produced nitric oxide may act as an antiviral agent but can also be toxic to host tissue.
