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Interplay of CCR2 signaling and local shear force determines vein graft neointimal hyperplasia in vivo
Author(s) -
Jiang Zhihua,
Yu Peng,
Tao Ming,
Ifantides Cristos,
Ozaki C. Keith,
Berceli Scott A.
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.10.015
Subject(s) - neointimal hyperplasia , ccr2 , chemokine , monocyte , microbiology and biotechnology , chemokine receptor , in vivo , hyperplasia , chemotaxis , receptor , chemistry , medicine , immunology , biology , restenosis , stent
Leukocytes play a central role in vein graft neointimal hyperplasia, which is significantly augmented under low shear conditions. The current concept is that shear force regulates leukocyte adhesion predominately through up‐regulation of chemokines and growth factors within the graft wall. Using rabbit and murine vein graft models, we demonstrate that CC chemokine receptor 2/monocyte chemoattractant protein‐1 mediated monocyte recruitment and a low shear environment act synergistically to augment neointimal hyperplasia development and removal of either of the conditions leads to a significant reduction in neointimal thickening. We propose a novel concept that the shear stress response element phenotypically stems from the complex interplay of the biological and physical microenvironments.