The promotion of tissue engineering blood vessel patency by CGS21680 through regulating pro-inflammatory activities of endothelial progenitor cell

The promotion of tissue engineering blood vessel patency by CGS21680 through regulating pro-inflammatory activities of endothelial progenitor cell
复制标题

CGS21680通过调节内皮祖细胞的促炎活性促进组织工程血管通畅。

DOI:
10.1002/jbm.a.36457
复制
发表时间:
2018-10-01
影响因子:
4.9
通讯作者:
Zhu, Chuhong
Zhu, Chuhong
中科院分区:
工程技术3区
文献类型:
--
作者:
Chen, Wen;Xiao, Li;Zhu, Chuhong

文献摘要

被引文献

相似文献

内皮祖细胞的动员和归巢是组织工程血管快速内皮化的关键。炎症可影响TEBV通畅性,并且单核细胞/巨噬细胞(MM)是主要的效应细胞。但目前尚不清楚TEBV移植后EPCs与MM的相互作用。我们的研究结果表明,脱细胞材料不会直接引起急性和严重的炎症反应,但激活归巢EPCs中的E-选择素表达,逐渐促进MM向M1的极化。腺苷A2 a受体激动剂CGS 21680促进MM分泌更多促血管生成因子,诱导EPC迁移和动员。CGS 21680可通过下调EPC促炎分子如E-selectin抑制MM向M1型的极化。制备了壳聚糖/(2-羟丙基)-β-环糊精纳米粒,并通过层层组装将其修饰为TEBV。动物实验表明,该支架可保持通畅6个月,并观察到良好的内皮化。总之,我们的研究结果表明,EPC促炎活性的调节是一种新的途径,以提高TEBV通畅性。(c)2018 Wiley Periodicals,Inc. J Biomed Mater Res Part A:106A:2634-2642,2018.
The mobilization and homing of endothelial progenitor cells (EPCs) contribute to the rapid endothelialization of tissue engineering blood vessel (TEBV). Inflammation can affect TEBV patency, and monocytes/macrophages (MM) are the main effector cells. But it is not clear how EPCs interact with MM after TEBV transplantation. Our results showed acellular materials would not directly cause acute and severe inflammatory responses but activate E-selectin expression in homing EPCs, gradually promoting the polarization of MM to the M1. Adenosine A2a receptor agonist CGS21680 promoted the secretion of more proangiogenic factors from MM, inducing EPC migration and mobilization. CGS21680 could inhibit MM polarization to the M1 type through the down-regulation of EPC proinflammatory molecules, such as E-selectin. Chitosan/(2-hydroxypropyl)--cyclodextrin nanoparticles were prepared to control the release of CGS-21680 and then modified to TEBVs through layer-by-layer assembly. Animal experiments showed that this TEBV can maintain patency for 6 months and good endothelialization was observed. In summary, our results showed the regulation of EPC pro-inflammatory activities is a new approach to enhance TEBV patency. (c) 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 2634-2642, 2018.