Genetically engineered excitable cardiac myofibroblasts coupled to cardiomyocytes rescue normal propagation and reduce arrhythmia complexity in heterocellular monolayers.

ABSTRACT:

Rationale and objective

The use of genetic engineering of unexcitable cells to enable expression of gap junctions and inward rectifier potassium channels has suggested that cell therapies aimed at establishing electrical coupling of unexcitable donor cells to host cardiomyocytes may be arrhythmogenic. Whether similar considerations apply when the donor cells are electrically excitable has not been investigated. Here we tested the hypothesis that adenoviral transfer of genes coding Kir2.1 (I(K1)), Na(V)1.5 (I(Na)) and connexin-43 (Cx43) proteins into neonatal rat ventricular myofibroblasts (NRVF) will convert them into fully excitable cells, rescue rapid conduction velocity (CV) and reduce the incidence of complex reentry arrhythmias in an in vitro model.

Methods and results

SUBMITTER: Hou L 

PROVIDER: S-EPMC3564921 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature