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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 I2 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 I2 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 I2-IP system is essential for EPCs to accomplish their function and plays a critical role in the regulation of vascular remodeling.

(C) 2010 American Heart Association, Inc.