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Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
09:40

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Published on: May 13, 2019

Cardiac-specific NRAP overexpression causes right ventricular dysfunction in mice.

Shajia Lu1, Garland L Crawford, Justin Dore

  • 1National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA.

Experimental Cell Research
|February 1, 2011
PubMed
Summary

Chronic overexpression of cardiac NRAP protein causes right ventricular cardiomyopathy in mice. This finding suggests NRAP upregulation is not the primary cause of dilated cardiomyopathy in other models.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cardiac Remodeling

Background:

  • Nuclear Receptor Activity Modulating Protein (NRAP) is a muscle-specific protein crucial for myofibril assembly.
  • NRAP is localized to cardiac intercalated disks and its expression is elevated in early stages of dilated cardiomyopathy models.
  • The precise role of NRAP in cardiac function and disease pathogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the functional consequences of chronic cardiac-specific NRAP overexpression in vivo.
  • To determine if elevated NRAP levels contribute to cardiac dysfunction and remodeling.
  • To elucidate the potential role of NRAP in the pathogenesis of dilated cardiomyopathy.

Main Methods:

  • Development of novel transgenic mouse lines with cardiac-specific NRAP overexpression using a tet-off system.
  • Assessment of cardiac structure and function via echocardiography at 40-50 weeks of age.
  • Analysis of gene expression for markers of cardiac stress and evaluation of key intercalated disk proteins (N-cadherin, connexin-43).

Main Results:

  • Cardiac-specific NRAP overexpression led to significant right ventricular dilation and reduced ejection fraction by 40-50 weeks.
  • Left ventricular function was minimally affected by NRAP overexpression.
  • Upregulation of brain natriuretic peptide and skeletal α-actin transcripts indicated a cardiomyopathic response in the right ventricle.
  • NRAP overexpression did not alter N-cadherin or connexin-43 levels or organization.

Conclusions:

  • Chronic NRAP overexpression induces right ventricular cardiomyopathy in mice.
  • The observed NRAP upregulation in other dilated cardiomyopathy models is unlikely to be the primary driver of left ventricular dysfunction or intercalated disk remodeling.
  • NRAP's role in cardiac pathology may be context-dependent and primarily impacts right ventricular function under chronic overexpression conditions.