Bone marrow monocyte lineage cells adhere on injured endothelium in a XXXX -dependent manner and accelerate reendothelialization as endothelial progenitor cells.

@entity1 @entity878 @entity5750 @entity3545 @entity1373 @entity2279 @entity2842 @entity1583 @entity2393 @entity35 @entity2280 @entity130
Peripheral blood (PB)-derived @entity5750 + monocytes were shown to transdifferentiate into endothelial cell (EC) lineage cells and contribute to neovascularization. We investigated whether bone marrow (BM)- or PB-derived @entity2280 -/ @entity5750 + cells are involved in reendothelialization after @entity130 . Although neither @entity1583 nor mesenchymal stem cells were included in @entity1 @entity5750 + monocyte lineage cells (BM-MLCs), they expressed EC-specific markers ( @entity878 , @entity2279 , @entity3545 , and endoglin) to an extent identical to mature ECs. When BM-MLCs were cultured with vascular endothelial growth factors, @entity1583 markers were drastically decreased and new EC-specific markers (Flk and @entity2280 ) were induced. BM-MLCs were intra-arterially transplanted into balloon-injured arteries of athymic nude @entity35 . When BM-MLCs were activated by @entity2842 ( @entity2842 ) in vivo or in vitro, they adhered onto injured endothelium, differentiated into EC-like cells by losing @entity1583 markers, and @entity1373 . Ability to prevent neointimal @entity1373 was more efficient than that of BM-derived @entity2280 + cells. MCP-dependent adhesion was not observed in PB-derived @entity2280 -/ @entity5750 + monocytes. Regenerated endothelium exhibited a cobblestone appearance, blocked extravasation of dye, and induced NO-dependent vasorelaxation. Basal adhesive activities on HUVECs under laminar flow and @entity2393 expression (basal and active forms) were significantly increased in BM-MLCs compared with PB-derived monocytes. @entity2842 markedly enhanced adhesive activity of BM-MLCs (2.8-fold) on HUVECs by activating @entity2393 conformation. Thus, BM-MLCs can function as EC progenitors that are more potent than @entity2280 + cells and acquire the ability to adhere on injured endothelium in a @entity2842 -dependent manner, leading to reendothelialization associated with inhibition of intimal @entity1373 . This will open a novel window to @entity2842 -mediated biological actions and vascular regeneration strategies by cell therapy.
