Vossler John D, Min Ju Young, Williams J Koudy, Goldstein Steven, Hamlin James, Lee Sang Jin, Yoo James J, Atala Anthony
Wake Forest Institute for Regenerative Medicine and, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. Department of General Surgery, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
Biomed Mater. 2015 Sep 3;10(5):055001. doi: 10.1088/1748-6041/10/5/055001.
The long term efficacy of tissue based heart valve grafts may be limited by progressive degeneration characterized by immune mediated inflammation and calcification. To avoid this degeneration, decellularized heart valves with functionalized surfaces capable of rapid in vivo endothelialization have been developed. The aim of this study is to examine the capacity of CD133 antibody-conjugated valve tissue to capture circulating endothelial progenitor cells (EPCs). Decellularized human pulmonary valve tissue was conjugated with CD133 antibody at varying concentrations and exposed to CD133 expressing NTERA-2 cl.D1 (NT2) cells in a microflow chamber. The amount of CD133 antibody conjugated on the valve tissue surface and the number of NT2 cells captured in the presence of shear stress was measured. Both the amount of CD133 antibody conjugated to the valve leaflet surface and the number of adherent NT2 cells increased as the concentration of CD133 antibody present in the surface immobilization procedure increased. The data presented in this study support the hypothesis that the rate of CD133(+) cell adhesion in the presence of shear stress to decellularized heart valve tissue functionalized by CD133 antibody conjugation increases as the quantity of CD133 antibody conjugated to the tissue surface increases.
基于组织的心脏瓣膜移植物的长期疗效可能会受到以免疫介导的炎症和钙化为特征的进行性退变的限制。为避免这种退变，已开发出具有能够在体内快速内皮化的功能化表面的去细胞心脏瓣膜。本研究的目的是检测与CD133抗体偶联的瓣膜组织捕获循环内皮祖细胞（EPC）的能力。将去细胞化的人肺动脉瓣膜组织与不同浓度的CD133抗体偶联，并在微流控腔室中暴露于表达CD133的NTERA-2 cl.D1（NT2）细胞。测量瓣膜组织表面偶联的CD133抗体的量以及在剪切应力存在下捕获的NT2细胞的数量。随着表面固定过程中存在的CD133抗体浓度增加，偶联到瓣膜小叶表面的CD133抗体的量和贴壁NT2细胞的数量均增加。本研究中呈现的数据支持这样的假设，即随着偶联到组织表面的CD133抗体数量增加，在剪切应力存在下CD133（+）细胞与通过CD133抗体偶联功能化的去细胞心脏瓣膜组织的粘附速率增加。
