Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Remodeling the mammalian heart using transgenesis

J Palermo1, J Gulick, W Ng

  • 1Division of Molecular Cardiovascular Biology, Children's Hospital Research Foundation, Cincinnati, OH 45267, USA.

Cellular & Molecular Biology Research
|January 1, 1995
PubMed
Summary

Transgenesis can alter mouse heart contractile proteins. Ectopic expression of myosin light chain 2 ventricular isoform (MLC2v) in the atrium impairs heart function, demonstrating compartment-specific replacement effects.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Molecular mechanics of cardiac myosin-binding protein C in native thick filaments.

Science (New York, N.Y.)·2012
Same author

Benign myoepithelioma of the lung: a case report and review of the literature.

Archives of pathology & laboratory medicine·2001
Same author

A familial hypertrophic cardiomyopathy alpha-tropomyosin mutation causes severe cardiac hypertrophy and death in mice.

Journal of molecular and cellular cardiology·2001
Same author

Altered SR protein expression associated with contractile dysfunction in diabetic rat hearts.

American journal of physiology. Heart and circulatory physiology·2001
Same author

Examining the in vivo role of the amino terminus of the essential myosin light chain.

The Journal of biological chemistry·2001
Same author

Mouse model of desmin-related cardiomyopathy.

Circulation·2001

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genetic Engineering

Background:

  • The heart's contractile function relies on specific myosin light chain (MLC2) isoforms.
  • Understanding how to manipulate these isoforms is crucial for studying cardiac physiology and disease.

Purpose of the Study:

  • To investigate if transgenesis can modify the mouse heart's contractile protein composition.
  • To determine the effects of ectopically expressing the ventricular MLC2 isoform (MLC2v) in the atrium.

Main Methods:

  • Utilized a mouse myosin heavy chain gene promoter (alpha-MyHC) for targeted gene expression.
  • Employed transgenic mice to overexpress MLC2v cDNA in cardiac atria and ventricles.
  • Assessed contractile protein stoichiometry and cardiac function using whole working heart preparations.

Related Experiment Videos

Main Results:

  • High-level transgene expression was achieved in both atria and ventricles, developmentally regulated.
  • Ectopic expression led to compartment-specific replacement of endogenous contractile proteins.
  • Overexpression of MLC2v in the atrium, where MLC2a is normally present, severely impaired contractile function.
  • Expression of MLC2v in the ventricle, its native compartment, did not alter endogenous protein levels despite high transcript accumulation.

Conclusions:

  • Transgenesis is a viable method to modify cardiac contractile protein composition.
  • Aberrant expression of MLC2 isoforms can significantly disrupt myocardial contractility.
  • MLC2 isoform stoichiometry is critical for maintaining normal cardiac performance.