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The promotion of tissue engineering blood vessel patency by CGS21680 through regulating pro‐inflammatory activities of endothelial progenitor cell
Author(s) -
Chen Wen,
Xiao Li,
Bai Jian,
Zeng Wen,
Yang Mingcan,
Shi Bingyi,
Zhu Chuhong
Publication year - 2018
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.36457
Subject(s) - progenitor cell , homing (biology) , proinflammatory cytokine , chemokine , inflammation , materials science , microbiology and biotechnology , cancer research , stem cell , medicine , immunology , biology , ecology
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)‐β‐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. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 2634–2642, 2018.