BioProject

Leukocyte flux contributes to thrombus formation in deep veins under pathologic conditions, but mechanisms which inhibit venous thrombosis are incompletely understood. More...

Leukocyte flux contributes to thrombus formation in deep veins under pathologic conditions, but mechanisms which inhibit venous thrombosis are incompletely understood. Ectonucleotide di(tri)phosphohydrolase 1 (ENTPD1 or Cd39), an ectoenzyme which 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. Gene expression profiling of WT 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. Overall design: C57BLK6 and CD39 null mice on a C57BLK6 background were either IVC ligated for 48hrs or were shammed. RNA was extracted and hybridized on Affymetrix microarrays. We obtained a n= 4 per group for biological replicates. Technical replication was achieved by pooling four samples for each of the four groups for analysis. We sought to detect gene expression changes at 48 hours following venous stasis-induced thrombosis. Less...