Premium
Mesenchymal stem cell seeding promotes reendothelialization of the endovascular stent
Author(s) -
Wu Xue,
Wang Guixue,
Tang Chaojun,
Zhang Dechuan,
Li Zhenggong,
Du Dingyuan,
Zhang Zhengcai
Publication year - 2011
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.33133
Subject(s) - restenosis , mesenchymal stem cell , stent , materials science , intimal hyperplasia , biomedical engineering , polylysine , medicine , surgery , smooth muscle , pathology , biology , biochemistry
This study is designed to make a novel cell seeding stent and to evaluate reendothelialization and anti‐restenosis after the stent implantation. In comparison with cell seeding stents utilized in previous studies, Mesenchymal stem cells (MSCs) have advantages on promoting of issue repair. Thus it was employed to improve the reendothelialization effects of endovascular stent in present work. MSCs were isolated by density gradient centrifugation and determined as CD29 + CD44 + CD34 − cells by immunofluorescence and immunocytochemistry; gluten and polylysine coated stents were prepared by ultrasonic atomization spray, and MSCs seeded stents were made through rotation culture according to the optimized conditions that were determined in previous studies. The results from animal experiments, in which male New Zealand white rabbits were used, show that the reendothelialization of MSCs coated stents can be completed within one month; in comparison with 316L stainless steel stents (316L SS stents) and gluten and polylysine coated stents, the intimal hyperplasia and in‐stent restenosis are significantly inhibited by MSCs coated stents. Endovascular stent seeded with MSCs promotes reendothelialization and inhibits the intimal hyperplasia and in‐stent restenosis compared with the 316L SS stents and the gluten and polylysine coated stents. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A: , 2011.