C-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction.

ABSTRACT:

Objectives

The aim of this study was to evaluate the role of tyrosine kinase cellular-Src (c-Src) inhibition on connexin43 (Cx43) regulation in a mouse model of myocardial infarction (MI).

Background

MI is associated with decreased expression of Cx43, the principal gap junction protein responsible for propagating current in ventricles. Activated c-Src has been linked to Cx43 dysregulation.

Methods

MI was induced in 12-week-old mice by coronary artery occlusion. MI mice were treated with c-Src inhibitors (PP1 or AZD0530), PP3 (an inactive analogue of PP1), or saline. Treated hearts were compared to sham mice by echocardiography, optical mapping, telemetry electrocardiographic monitoring, and inducibility studies. Tissues were collected for immunoblotting, quantitative

SUBMITTER: Rutledge CA 

PROVIDER: S-EPMC3963804 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature