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

Modulation of connexin43 expression: effects on cellular coupling

L M Davis1, J E Saffitz, E C Beyer

  • 1Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.

Journal of Cardiovascular Electrophysiology
|February 1, 1995
PubMed
Summary

Altering connexin43 (a major cardiac connexin) expression in cells impacts intercellular coupling. This study developed models to manipulate connexin43 levels, showing specific changes in cell communication without affecting other connexins.

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

Quantifying center of pressure variability in chondrodystrophoid dogs.

Veterinary journal (London, England : 1997)·2017
Same author

The E368Q Mutant Allele of <i>GJA8</i> is Associated with Congenital Cataracts with Intrafamilial Variation in a South Indian Family.

Open access journal of ophthalmology·2017
Same author

Myocyte interconnections at gap junctions and the development of anatomic substrates of ventricular arrhythmia's.

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology·2015
Same author

On the potential of hydrated storage for naturally derived ECMs and associated effects on mechanical and cellular performance.

Journal of biomedical materials research. Part B, Applied biomaterials·2013
Same author

Incidence of extrinsic compression of the internal jugular vein in unselected patients undergoing CT angiography.

AJNR. American journal of neuroradiology·2012
Same author

Counting single chromophore molecules for ultrasensitive analysis and separations on microchip devices.

Analytical chemistry·2011

Area of Science:

  • Cardiovascular Biology
  • Cellular Physiology
  • Molecular Biology

Background:

  • Gap junctions, formed by connexin proteins, are crucial for cardiac myocyte electrical signal propagation.
  • Connexin type and arrangement influence electrical resistance, conduction velocity, and arrhythmia risk.
  • Understanding connexin function is key to addressing cardiac electrical disorders.

Purpose of the Study:

  • To create genetically manipulable cell models for studying connexin43 (a major cardiac connexin).
  • To investigate the impact of altered connexin43 expression on intercellular coupling.
  • To examine if modifying connexin43 affects the expression of other connexin proteins.

Main Methods:

  • Stable transfection of BHK (poorly coupled) and BWEM (well coupled) cells with connexin43 cDNA in sense and antisense orientations.

Related Experiment Videos

  • Confirmation of transcript expression via RNA blots and protein levels via immunoblots.
  • Assessment of cell coupling by microinjecting Lucifer yellow dye and quantifying intercellular transfer.

    • Main Results:

    • Connexin43 protein levels were successfully altered in BHK cells (reduced in antisense, increased in sense transfectants).
    • Connexin43 manipulation did not affect connexin45 expression or induce other connexin mRNAs.
    • Significant changes in dye transfer (intercellular coupling) were observed in BHK cells, correlating with connexin43 levels, but not in BWEM cells.

    Conclusions:

    • Genetically manipulating connexin43 expression can alter cellular coupling.
    • These models allow for specific modulation of connexin43 without compensatory changes in the connexin phenotype.
    • This approach provides a foundation for future strategies to modify intercellular resistance in cardiac tissues.