Tuning the Thromboinflammatory Response to Venous Flow Interruption by the Ectonucleotidase CD39

Arteriosclerosis, Thrombosis, and Vascular Biology
Anuli C AnyanwuDavid J Pinsky

Abstract

Objective- Leukocyte flux contributes to thrombus formation in deep veins under pathological conditions, but mechanisms that inhibit venous thrombosis are incompletely understood. Ectonucleotide di(tri)phosphohydrolase 1 ( ENTPD1 or Cd39), an ectoenzyme that catabolizes extracellular adenine nucleotides, is embedded on the surface of endothelial cells and leukocytes. We hypothesized that under venous stasis conditions, CD39 regulates inflammation at the vein:blood interface in a murine model of deep vein thrombosis. Approach and Results- CD39-null mice developed significantly larger venous thrombi under venous stasis, with more leukocyte recruitment compared with wild-type mice. Gene expression profiling of wild-type and Cd39-null mice revealed 76 differentially expressed inflammatory genes that were significantly upregulated in Cd39-deleted mice after venous thrombosis, and validation experiments confirmed high expression of several key inflammatory mediators. P-selectin, known to have proximal involvement in venous inflammatory and thrombotic events, was upregulated in Cd39-null mice. Inferior vena caval ligation resulted in thrombosis and a corresponding increase in both P-selectin and VWF (von Willebrand Factor) levels whic...Continue Reading

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Citations

Apr 23, 2020·Arteriosclerosis, Thrombosis, and Vascular Biology·Xian LiJeremy P Wood
Feb 23, 2020·Frontiers in Pharmacology·Elisabetta CaiazzoCarla Cicala
Mar 20, 2021·Molecular and Cellular Biochemistry·Maria Luiza Mukai FranciosiAndréia Machado Cardoso
Oct 13, 2020·International Immunopharmacology·Jianrui ZengHuabao Xiong
Apr 9, 2021·Arteriosclerosis, Thrombosis, and Vascular Biology·Vijay KondreddyUsha R Pendurthi
Jun 11, 2021·Circulation Research·Meaghan E CollingYogendra Kanthi

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