Submit a comment

Ectonucleotidase CD39-driven control of postinfarction myocardial repair and rupture
Nadia R. Sutton, Takanori Hayasaki, Matthew C. Hyman, Anuli C. Anyanwu, Hui Liao, Danica Petrovic-Djergovic, Linda Badri, Amy E. Baek, Natalie Walker, Keigo Fukase, Yogendra Kanthi, Scott H. Visovatti, Ellen L. Horste, Jessica J. Ray, Sascha N. Goonewardena, David J. Pinsky
Nadia R. Sutton, Takanori Hayasaki, Matthew C. Hyman, Anuli C. Anyanwu, Hui Liao, Danica Petrovic-Djergovic, Linda Badri, Amy E. Baek, Natalie Walker, Keigo Fukase, Yogendra Kanthi, Scott H. Visovatti, Ellen L. Horste, Jessica J. Ray, Sascha N. Goonewardena, David J. Pinsky
View: Text | PDF
Research Article Cardiology Immunology

Ectonucleotidase CD39-driven control of postinfarction myocardial repair and rupture

Abstract

Mechanical complications of myocardial infarction (MI) are often fatal. Little is known about endogenous factors that predispose to myocardial rupture after MI. Ectonucleoside triphosphate diphosphohydrolase (CD39) could be a critical mediator of propensity to myocardial rupture after MI due to its role in modulating inflammation and thrombosis. Using a model of permanent coronary artery ligation, rupture was virtually abrogated in cd39–/– mice versus cd39+/+ controls, with elevated fibrin and collagen deposition and marked neutrophil and macrophage influx. Macrophages were found to display increased surface expression of CD301 and CD206, marking a reparative phenotype, driven by increased extracellular ATP and IL-4 in the infarcted myocardium of cd39–/– mice. A myeloid-specific CD39-knockout mouse also demonstrated protection from rupture, with an attenuated rupture phenotype, suggesting that complete ablation of CD39 provides the greatest degree of protection in this model. Absence of CD39, either globally or in a myeloid lineage–restricted fashion, skews the phenotype toward alternatively activated (reparative) macrophage infiltration following MI. These studies reveal a previously unrecognized and unexpected role of endogenous CD39 to skew macrophage phenotype and promote a propensity to myocardial rupture after MI.

Authors

Nadia R. Sutton, Takanori Hayasaki, Matthew C. Hyman, Anuli C. Anyanwu, Hui Liao, Danica Petrovic-Djergovic, Linda Badri, Amy E. Baek, Natalie Walker, Keigo Fukase, Yogendra Kanthi, Scott H. Visovatti, Ellen L. Horste, Jessica J. Ray, Sascha N. Goonewardena, David J. Pinsky

×

Guidelines

The Editorial Board will only consider comments that are deemed relevant and of interest to readers. The Journal will not post data that have not been subjected to peer review; or a comment that is essentially a reiteration of another comment.

  • Comments appear on the Journal’s website and are linked from the original article’s web page.
  • Authors are notified by email if their comments are posted.
  • The Journal reserves the right to edit comments for length and clarity.
  • No appeals will be considered.
  • Comments are not indexed in PubMed.

Specific requirements

  • Maximum length, 400 words
  • Entered as plain text or HTML
  • Author’s name and email address, to be posted with the comment
  • Declaration of all potential conflicts of interest (even if these are not ultimately posted); see the Journal’s conflict-of-interest policy
  • Comments may not include figures
This field is required
This field is required
This field is required
This field is required
This field is required
This field is required