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Monocyte adhesion and endothelial hyperpermeability are associated with failure of arteriovenous fistula (AVF) maturation for hemodialysis access
Author(s) -
Lee Eugene S,
Shen Qiang,
Guo Mingzhang,
Pitts Robert L,
Wu Mack H,
Yuan Sarah Y
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.590.5
Subject(s) - monocyte , medicine , arteriovenous fistula , endothelium , cell adhesion molecule , adhesion , immunology , hemodialysis , cd11c , peripheral , vascular permeability , biology , surgery , chemistry , phenotype , biochemistry , organic chemistry , gene
Leukocyte‐endothelium interactions play an important role in vascular remodeling. The aim of this study was to test the hypothesis that monocyte adhesion‐induced endothelial hyperpermeability hampers vascular graft remodeling and maturation leading to AVF failure. Monocytes were isolated from 5 patients with successful AVF and 5 patients with failure of AVF maturation. The expression of adhesion molecules was measured using flow cytometry. In parallel, monocyte transendothelial migration and its associated endothelial permeability were assessed in a monocyte‐HUVEC co‐culture model. Compared to monocytes from the group with successful AVF, monocytes obtained from patients with AVF failure had significantly higher levels of CD11c expression and trans‐endothelial migration. Monocytes from patients with failed AVF induced a further decrease in transendothelial electric resistance. The data suggest that monocyte adhesion and endothelial hyperpermeability contribute to the failure of AVF maturation. This work was supported by R01 HL061507, HL084542, and a Peripheral Vascular Surgery Society Grant.