Optical action potential mapping in acute models of ischemia–Reperfusion injury: Probing the arrhythmogenic role of the mitochondrial translocator protein

Zeki Ilkan, Benjamin Strauss, Chiara Campana, Fadi G. Akar

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

5 Scopus citations

Abstract

Ischemia–reperfusion (I/R) injury causes dynamic changes in electrophysiological properties that promote the incidence of post-ischemic arrhythmias. High-resolution optical action potential mapping allows for a quantitative assessment of the electrophysiological substrate at a cellular resolution within the intact heart, which is critical for elucidation of arrhythmia mechanisms. We and others have found that pharmacological inhibition of the translocator protein (TSPO) is highly effective against postischemic arrhythmias. A major hurdle that has limited the translation of this approach to patients is the fact that available TSPO ligands have several confounding effects, including a potent negative ionotropic property. To circumvent such limitations we developed an in vivo cardiac specific TSPO gene silencing approach as an alternative. Here, we provide the methodological details of our optical action potential mapping studies that were designed to probe the effects of TSPO silencing in hearts from spontaneously hypertensive rats (SHR) that are prone to I/R injury.

Original languageEnglish
Title of host publicationMethods in Molecular Biology
PublisherHumana Press Inc.
Pages133-143
Number of pages11
DOIs
StatePublished - 2018

Publication series

NameMethods in Molecular Biology
Volume1816
ISSN (Print)1064-3745

Keywords

  • Adeno-associated virus
  • Arrhythmia
  • Gene therapy
  • Mitochondria
  • Optical mapping
  • Translocator protein
  • shRNA

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