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Controlled autologous recellularization and inhibited degeneration of decellularized vascular implants by side-specific coating with stromal cell-derived factor 1α and fibronectin.
Biomedical Materials ( IF 3.9 ) Pub Date : 2020-04-29 , DOI: 10.1088/1748-605x/ab54e3
Yukiharu Sugimura 1 , Agunda Chekhoeva , Kyohei Oyama , Sentaro Nakanishi , Mahfuza Toshmatova , Shunsuke Miyahara , Mareike Barth , Anna Kathrin Assmann , Artur Lichtenberg , Alexander Assmann , Payam Akhyari
Affiliation  

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.

中文翻译:

通过用基质细胞衍生因子 1α 和纤连蛋白进行侧特异性涂层控制自体再细胞化和抑制脱细胞血管植入物的变性。

优化的生物相容性对于心血管植入物的耐用性至关重要。以前,纤维连接蛋白 (FN) 和基质细胞衍生因子 1α (SDF1α) 的组合涂层已被证明可以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管腔 SDF1α 涂层和外膜 FN 涂层对脱细胞大鼠主动脉植入物的体内细胞化和变性的影响。主动脉弓血管供体移植物是去污剂去细胞的。管腔移植物表面涂有 SDF1α,而外膜表面涂有 FN。将 SDF1α 涂层和未涂层​​的移植物通过肾下移植 (n = 20) 并随访至八周。两周后腔内 SDF1α 涂层加速了细胞内膜群体(92.4 ± 2.95% 与对照组的 61.1 ± 6.51%,p < 0.001)。SDF1α 涂层抑制新内膜增生,导致八周后内膜与中膜的比率显着降低(0.62 ± 0.15 与对照组的 1.35 ± 0.26,p < 0.05)。此外,在第 8 周时,与对照组相比,SDF1α 组的中膜钙化显着减少(近端弓区的钙化面积 1092 ± 517 μm2 与 11 814 ± 1883 μm2,p < 0.01)。具有 SDF1α 的管腔涂层促进体内早期自体内膜再细胞化,并减弱新内膜增生以及脱细胞血管移植物的钙化。SDF1α 涂层抑制新内膜增生,导致八周后内膜与中膜的比率显着降低(0.62 ± 0.15 与对照组的 1.35 ± 0.26,p < 0.05)。此外,在第 8 周时,与对照组相比,SDF1α 组的中膜钙化显着减少(近端弓区的钙化面积 1092 ± 517 μm2 与 11 814 ± 1883 μm2,p < 0.01)。具有 SDF1α 的管腔涂层促进体内早期自体内膜再细胞化,并减弱新内膜增生以及脱细胞血管移植物的钙化。SDF1α 涂层抑制新内膜增生,导致八周后内膜与中膜的比率显着降低(0.62 ± 0.15 与对照组的 1.35 ± 0.26,p < 0.05)。此外,在第 8 周时,与对照组相比,SDF1α 组的中膜钙化显着减少(近端弓区的钙化面积 1092 ± 517 μm2 与 11 814 ± 1883 μm2,p < 0.01)。具有 SDF1α 的管腔涂层促进体内早期自体内膜再细胞化,并减弱新内膜增生以及脱细胞血管移植物的钙化。与对照组相比,SDF1α 组的中膜钙化显着减少(近端弓区钙化面积 1092 ± 517 μm2 与 11 814 ± 1883 μm2,p < 0.01)。具有 SDF1α 的管腔涂层促进体内早期自体内膜再细胞化,并减弱新内膜增生以及脱细胞血管移植物的钙化。与对照组相比,SDF1α 组的中膜钙化显着减少(近端弓区钙化面积 1092 ± 517 μm2 与 11 814 ± 1883 μm2,p < 0.01)。具有 SDF1α 的管腔涂层促进体内早期自体内膜再细胞化,并减弱新内膜增生以及脱细胞血管移植物的钙化。
更新日期:2020-04-28
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