Optimized biocompatibility is crucial for the durability of cardiovascular implants. Previously, a combined coating with fibronectin (FN) and stromal cell-derived factor 1α (SDF1α) has been shown to accelerate the in vivo cellularization of synthetic vascular grafts and to reduce the calcification of biological pulmonary root grafts. In this study, we evaluate the effect of side-specific luminal SDF1α coating and adventitial FN coating on the in vivo cellularization and degeneration of decellularized rat aortic implants. Aortic arch vascular donor grafts were detergent-decellularized. The luminal graft surface was coated with SDF1α, while the adventitial surface was coated with FN. SDF1α-coated and uncoated grafts were infrarenally implanted (n = 20) in rats and followed up for up to eight weeks. Cellular intima population was accelerated by luminal SDF1α coating at two weeks (92.4 ± 2.95% versus 61.1 ± 6.51% in controls, p < 0.001). SDF1α coating inhibited neo-intimal hyperplasia, resulting in a significantly decreased intima-to-media ratio after eight weeks (0.62 ± 0.15 versus 1.35 ± 0.26 in controls, p < 0.05). Furthermore, at eight weeks, media calcification was significantly decreased in the SDF1α group as compared to the control group (area of calcification in proximal arch region 1092 ± 517 μm2 versus 11 814 ± 1883 μm2, p < 0.01). Luminal coating with SDF1α promotes early autologous intima recellularization in vivo and attenuates neo-intima hyperplasia as well as calcification of decellularized vascular grafts.

译文

优化的生物相容性对于心血管植入物的耐久性至关重要。以前,已显示具有纤连蛋白 (FN) 和基质细胞衍生因子1α (SDF1α) 的组合涂层可加速合成血管移植物的体内细胞化并减少生物肺根移植物的钙化。在这项研究中,我们评估了侧特异性腔SDF1α 涂层和外膜FN涂层对脱细胞大鼠主动脉植入物体内细胞化和变性的影响。主动脉弓血管供体移植物被去污剂脱细胞。腔移植物表面涂有SDF1α,而外膜表面涂有FN。将sdf1α 涂层和未涂层的移植物在大鼠体内植入 (n = 20),并进行长达八周的随访。在两周时,腔膜SDF1α 涂层加速了细胞内膜群 (对照组为92.4 ± 2.95%,对照组为61.1 ± 6.51%,p <0.001)。SDF1α 涂层抑制新内膜增生,导致8周后内膜与中膜比率显着降低 (对照组为0.62 ± 0.15,对照组为1.35 ± 0.26,p <0.05)。此外,与对照组相比,在8周时,SDF1α 组的介质钙化显着降低 (近端弓区域的钙化面积1092 ± 517 μm2与11 814 ± 1883 μm2相比,p <0.01)。带有SDF1α 的腔涂层可促进体内早期自体内膜再细胞化,并减轻新内膜增生以及脱细胞血管移植物的钙化。

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