Cardiac mitochondrial connexin 43 regulates apoptosis. Academic Article uri icon

Overview

abstract

  • Connexin 43 (Cx43) is thought to be present largely in the plasma membrane and its function solely to provide low resistance electrical connection between myocytes. A recent report suggested the presence of Cx43 in the mitochondria as well. We confirmed the presence of Cx43 in the mitochondria isolated from adult rat ventricles with the Cx43 immunoreactivity fractionating to the outer mitochondrial membrane. Mitochondrial Cx43 is mostly phosphorylated only detected by a phospho-specific antibody. Using a Ca2+ -sensitive electrode and Western blot, we showed that the gap junction inhibitors 18-beta-glycyrrhetinic acid (beta-GA), oleamide, and heptanol all induced concomitant release of Ca2+ and cytochrome C in isolated mitochondria whereas the inactive analog 18-beta-glycyrrhizic acid failed to do so. In low density neonatal myocyte culture with no appreciable cell-cell contacts, beta-GA induced apoptosis as assessed by TUNEL staining. Our results suggest a novel role of Cx43 as a regulator of mitochondrial physiology and myocyte apoptosis.

publication date

  • November 10, 2006

Research

keywords

  • Apoptosis
  • Connexin 43
  • Mitochondria, Heart
  • Myocardium

Identity

PubMed Central ID

  • PMC1829482

Scopus Document Identifier

  • 33751409127

Digital Object Identifier (DOI)

  • 10.1016/j.bbrc.2006.10.177

PubMed ID

  • 17107662

Additional Document Info

volume

  • 352

issue

  • 1