Distinct contribution of human cord blood-derived endothelial colony forming cells to liver and gut in a fetal sheep model.

Distinct contribution of human cord blood-derived endothelial colony forming cells to liver and gut in a fetal sheep model.
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人脐带血来源的内皮集落形成细胞对胎羊模型中肝脏和肠道的独特贡献。

DOI:
10.1002/hep.25753
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发表时间:
2012
期刊:
Hepatology (Baltimore, Md.)
影响因子:
--
通讯作者:
Almeida-Porada,Graca
Almeida-Porada,Graca
中科院分区:
--
文献类型:
--
作者:
Wood,JoshuaA;Colletti,Evan;Mead,LauraE;Ingram,David;Porada,ChristopherD;Zanjani,EsmailD;Yoder,MervinC;Almeida-Porada,Graca

文献摘要

相似文献

Although the vasculogenic potential of circulating and cord blood (CB)‐derived endothelial colony‐forming cells (ECFC) has been demonstratedin vitroandin vivo,little is known about the inherent biologic ability of these cells to home to different organs and contribute to tissue‐specific cell populations. Here we used a fetal sheep model ofin uterotransplantation to investigate and compare the intrinsic ability of human CB‐derived ECFC to migrate to the liver and to the intestine, and to define ECFC's intrinsic ability to integrate and contribute to the cytoarchitecture of these same organs. ECFCs were transplanted by an intraperitoneal or intrahepatic route (IH) into fetal sheep at concentrations ranging from 1.1‐2.6 × 106cells/fetus. Recipients were evaluated at 85 days posttransplant for donor (human) cells using flow cytometry and confocal microscopy. We found that, regardless of the route of injection, and despite the IH delivery of ECFC, the overall liver engraftment was low, but a significant percentage of cells were located in the perivascular regions and retained the expression of hallmark endothelial makers. By contrast, ECFC migrated preferentially to the intestinal crypt region and contributed significantly to the myofibroblast population. Furthermore, ECFC expressing CD133 and CD117 lodged in areas where endogenous cells expressed those same phenotypes.Conclusion:ECFC inherently constitute a potential source of cells for the treatment of intestinal diseases, but strategies to increase the numbers of ECFC persisting within the hepatic parenchyma are needed in order to enhance ECFC therapeutic potential for this organ. (HEPATOLOGY2012;56:1086–1096)