Human umbilical cord blood endothelial progenitor cells decrease vein graft neointimal hyperplasia in SCID mice.
Human umbilical cord blood endothelial progenitor cells decrease vein graft neointimal hyperplasia in SCID mice.
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DOI：
10.1016/j.atherosclerosis.2010.04.018
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发表时间：
2010-09
期刊：
影响因子：
5.3
通讯作者：
Dong, Chunming
中科院分区：
文献类型：
--
作者：
Zhu, Shoukang;Malhotra, Anuj;Zhang, Lisheng;Deng, Shanming;Zhang, Taifang;Freedman, Neil J.;Storms, Robert;Peppel, Karsten;Goldschmidt-Clermont, Pascal J.;Dong, Chunming
Vein graft endothelial damage is a key step in the development of neointimal hyperplasia, leading to vein graft failure. We sought to determine whether exogenous endothelial progenitor cells could promote vein graft re-endothelialization, and thereby ameliorate neointimal hyperplasia. Carotid artery interposition grafting was performed with syngeneic inferior vena cavae in mice with severe combined immunodeficiency (SCID). Lineage-negative human umbilical cord blood (hUCB) cells (or medium alone) were injected into vein-grafted mice intraoperatively and 2 weeks postoperatively. In vein grafts from hUCB cell-injected mice, we found human HLA-expressing endothelial cells, as well as increased levels of VEGF and FGF-2. Furthermore, hUCB cells secreted VEGF and FGF-2 in vitro. The markedly enhanced endothelial regeneration, likely resulting from both direct engraftment and paracrine actions of hUCB cells, inhibited inflammatory response, diminished intimal cell proliferation, and reduced neointimal hyperplasia in the vein grafts. hUCB cells may accelerate vein graft re-endothelialization via both direct differentiation into endothelial cells and release of paracrine factors to enhance endothelial regeneration and reduce inflammation. These data highlight a potential therapeutic role for cellular therapy in vessel injury.
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