期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 30, 期 3, 页码 464-U213出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.109.193730
关键词
vascular remodeling; prostaglandin I-2; endothelial progenitor cells; fibronectin; adhesion
资金
- Ministry of Education, Science, Sports, and Culture of Japan
- Takeda Science Foundation
- Akiyama Memorial Foundation
- Suhara Memorial Foundation
- Smoking Research Foundation
Objective-Endothelial progenitor cells (EPCs) play an important role in the self-healing of a vascular injury by participating in the reendothelialization that limits vascular remodeling. We evaluated whether prostaglandin I-2 plays a role in the regulation of the function of EPCs to limit vascular remodeling. Methods and Results-EPCs (Lin(-)cKit(+)Flk-1(+) cells) were isolated from the bone marrow (BM) of wild-type (WT) mice or mice lacking the prostaglandin I-2 receptor IP (IP-/- mice). Reverse transcription-polymerase chain reaction analysis showed that EPCs among BM cells specifically express IP. The cellular properties of EPCs, adhesion, migration, and proliferation on fibronectin were significantly attenuated in IP-deficient EPCs compared with WT EPCs. In contrast, IP agonists facilitated these functions in WT EPCs, but not in IP-deficient EPCs. The specific deletion of IP in BM cells, which was performed by transplanting BM cells of IP-/- mice to WT mice, accelerated wire injury-mediated neointimal hyperplasia in the femoral artery. Notably, transfused WT EPCs, but not IP-deficient EPCs, were recruited to the injured vessels, participated in reendothelialization, and efficiently rescued the accelerated vascular remodeling. Conclusion-These findings clearly indicate that the prostaglandin I-2-IP system is essential for EPCs to accomplish their function and plays a critical role in the regulation of vascular remodeling. (Arterioscler Thromb Vasc Biol. 2010;30:464-470.)
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