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Related Experiment Videos

Molecular and physiological alterations in murine ventricular dysfunction

H A Rockman1, S Ono, R S Ross

  • 1Department of Medicine, Veterans Affairs Hospital-San Diego, CA.

Proceedings of the National Academy of Sciences of the United States of America
|March 29, 1994
PubMed
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Researchers developed a mouse model for right ventricular dysfunction, a condition mimicking human pulmonary arterial hypertension. This model reveals early genetic markers like phospholamban down-regulation in failing hearts.

Area of Science:

  • Cardiovascular Research
  • Animal Models
  • Molecular Cardiology

Background:

  • Right ventricular (RV) dysfunction is a critical complication of pulmonary arterial hypertension (PAH).
  • Developing reliable animal models is essential for understanding RV failure mechanisms and testing therapies.
  • Current models may not fully recapitulate the chronic pressure overload and subsequent dysfunction seen in human PAH.

Purpose of the Study:

  • To establish and characterize a novel murine model of RV dysfunction induced by pulmonary artery constriction (PAC).
  • To quantitatively assess in vivo RV function using x-ray contrast microangiography.
  • To investigate molecular changes, including gene expression, associated with RV dysfunction in this model.

Main Methods:

  • Microsurgical pulmonary artery banding in mice to create graded levels of pressure overload.

Related Experiment Videos

  • X-ray contrast microangiography for in vivo assessment of RV volumes and ejection fraction.
  • Northern and immunoblot analyses to quantify phospholamban and SERCA2a protein and mRNA levels.

    • Main Results:

    • Severe PAC (14 days) induced RV dilatation, dysfunction, right atrial enlargement, and tricuspid regurgitation.
    • Moderate PAC led to RV hypertrophy with preserved function, demonstrating a dose-dependent response.
    • Both severe and moderate PAC significantly down-regulated phospholamban mRNA and protein; severe PAC also reduced SERCA2a protein.

    Conclusions:

    • This murine model effectively replicates key features of human RV dysfunction in chronic PAH.
    • Down-regulation of phospholamban serves as an early molecular marker for RV dysfunction.
    • The model provides a platform for investigating the role of genetic alterations in the development of heart failure phenotypes.