Human Endothelial Colony Forming Cells were transfected at 60 % confluence with SilenceMag and gene silencing was assessed 48 h after.
This article demonstres the capacity of Magnetofection technology to efficiently silence gene expression in vivo with siRNA using SilenceMag from OZ Biosciences.article reference: J Thromb Haemost. 2014 Mar 8.
Neutrophils recruit and activate Human Endothelial Colony Forming Cells at the site of vessel injury via PSGL-1 and L-Selectin.
Hubert L1, Darbousset R, Panicot-Dubois L, Robert S, Sabatier F, Fallague K, Dignat-George F, Dubois C.AbstractBACKGROUND: Endothelial colony-forming cells (ECFCs) represent a subpopulation of circulating endothelial progenitor cells that have been implicated in vascular repair. However, no study has evaluated the role of ECFCs in endothelial injury leading to thrombus formation.
OBJECTIVE: We investigated the kinetics, mechanisms and role of ECFCs recruitment in the dynamics of thrombus formation and stabilization.
METHODS AND RESULTS: Using digital intravital microscopy in living mice we show that ECFCs, but not mature endothelial cells, adhere to sites of laser-induced injury and do not affect the kinetics of thrombus formation. This interaction occurs once the platelet thrombus has been stabilized and is dependent on the presence of neutrophils but not platelets or fibrin. In vitro, the interaction of the activated neutrophils with activated endothelial cells is a prerequisite for the capture of ECFCs. Neutrophils activate ECFCs and increase their angiogenic properties, such as their ability to migrate and to form pseudo-capillaries. This new identified interaction of ECFCs with the neutrophils is mediated by the PSGL-1/L-selectin axis both in vitro and in vivo.
CONCLUSIONS: This study is the first demonstration that neutrophils present at the site of injury recruit ECFCs via PSGL-1/L-selectin. This interaction between neutrophils and ECFCs could play a key role in the regeneration of injured vessels in pathophysiological conditions. This article is protected by copyright. All rights reserved.
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