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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Composite scaffold provides a cell delivery platform for cardiovascular repair
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Composite scaffold provides a cell delivery platform for cardiovascular repair

机译：复合支架为心血管修复提供了细胞递送平台

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Control over cell engraftment, survival, and function remains critical for heart repair. We have established a tissue engineering platform for the delivery of human mesenchymal progenitor cells (MPCs) by a fully biological composite scaffold. Specifically, we developed a method for complete decellularization of human myocardium that leaves intact most elements of the extracellular matrix, as well as the underlying mechanical properties. A cell-matrix composite was constructed by applying fibrin hydrogel with suspended cells onto decellularized sheets of human myocardium. We then implanted this composite onto the infarct bed in a nude rat model of cardiac infarction. We next characterized the myogenic and vasculogenic potential of immunoselected human MPCs and demonstrated that in vitro conditioning with a low concentration of TGF-ft promoted an arteriogenic profile of gene expression. When implanted by composite scaffold, preconditioned MPCs greatly enhanced vascular network formation in the infarct bed by mechanisms involving the secretion of paracrine factors, such as SDF-1, and the migration of MPCs into ischemic myocardium, but not normal myocardium. Echocardiography demonstrated the recovery of baseline levels of left ventricular systolic dimensions and contractility when MPCs were delivered via composite scaffold. This adaptable platform could be readily extended to the delivery of other reparative cells of interest and used in quantitative studies of heart repair.
机译：控制细胞植入，存活和功能对于心脏修复仍然至关重要。我们已经建立了一个组织工程平台，用于通过完全生物的复合支架递送人间充质祖细胞（MPC）。具体而言，我们开发了一种使人心肌完全脱细胞的方法，该方法使完整的细胞外基质元素以及完整的机械性能得以保留。通过将具有悬浮细胞的纤维蛋白水凝胶施加到人心肌的脱细胞片上来构建细胞基质复合物。然后，我们将这种复合材料植入心脏梗死裸鼠模型中的梗死床上。接下来，我们表征了免疫选择的人MPC的成肌和血管生成潜能，并证明了低浓度TGF-ft的体外调节可促进基因表达的动脉生成。当用复合支架植入时，经过预处理的MPC通过涉及分泌旁分泌因子（例如SDF-1）的机制以及MPC迁移到缺血性心肌而非正常心肌中，从而大大增强了梗死床的血管网络形成。超声心动图显示，当通过复合支架递送MPC时，左心室收缩期尺寸和收缩力的基线水平已恢复。这个适应性强的平台可以很容易地扩展到其他感兴趣的修复细胞的传递，并用于心脏修复的定量研究。

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