Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)
165 Downloads (Pure)

Abstract

Background:

Increased reactive oxygen species (ROS) production is involved in the process of adverse cardiac remodeling and development of heart failure after myocardial infarction (MI). NADPH oxidase-2 (Nox2) is a major ROS source within the heart and its activity increases after MI. Furthermore, genetic deletion of Nox2 is protective against post-MI cardiac remodeling. Nox2 levels may increase both in cardiomyocytes and endothelial cells and recent studies indicate cell-specific effects of Nox2, but it is not known which of these cell types is important in post-MI remodeling. 

Methods and results:

We have generated transgenic mouse models in which Nox2 expression is targeted either to cardiomyocytes (cardio-Nox2TG) or endothelial cells (endo-Nox2TG). We here studied the response of cardio-Nox2TG mice, endo-Nox2TG mice and matched wild-type littermates (WT) to MI induced by permanent left coronary artery ligation up to 4 weeks. Initial infarct size assessed by magnetic resonance imaging (MRI) and cardiac dysfunction were similar among groups. Cardiomyocyte hypertrophy and interstitial fibrosis were augmented in cardio-Nox2TG compared to WT after MI and post-MI survival tended to be worse whereas endo-Nox2TG mice showed no significant difference compared to WT. Conclusions These results indicate that cardiomyocyte rather than endothelial cell Nox2 may have the more important role in post-MI remodeling.

Original languageEnglish
Pages (from-to)11-17
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Volume98
Early online date7 Jul 2016
DOIs
Publication statusPublished - Sept 2016

Keywords

  • Cardiac remodeling
  • Heart failure
  • Myocardial infarction
  • NADPH oxidase
  • Reactive oxygen species

Fingerprint

Dive into the research topics of 'Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction'. Together they form a unique fingerprint.

Cite this