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Prostacyclin: a potential new target for endothelial progenitor cell-mediated angiogenesis.

action of PGI2 in EPC-mediated angiogenesis is not yet clear. He et al9 showed that cyclooxygenase (COX) enzymatic activity, and the subsequent production of PGI2, enhances EPCmediated angiogenesis by the PPARδ pathway. They showed that activation of the COX-1/PGI2/PPARδ pathway in EPCs resulted in the independent, direct differentiation of EPCs into endothelial cells through a PGI2-specific receptor, IP. Kawabe et al showed that removal of IP from EPCs caused their dysfunction10 and following that study, the same group, including Aburakawa et al, have described the critical role of the PGI2/IP signal in EPC-mediated angiogenesis.11 In this issue of the Journal, the authors compare the effects of PGI2/IP signaling in bone marrow and non-bone marrow tissues on blood flow recovery in hindlimb ischemia, using a bone marrow transplantation model in genetically IP-deficient mice. They observed that IP-deficient mice, after receiving a bone marrow transplant of wild-type cells, initially showed decreased blood flow, compared with wild-type mice in the hindlimb ischemia model; the decreased blood flow completely recovered within 30 days of the induction of hindlimb ischemia. In contrast, ince Asahara et al discovered endothelial progenitor cells (EPCs) in 1997,1 extensive studies have been conducted in an attempt to not only clarify and characterize these cells, but also to utilize EPC-containing products (ie, bone marrow-derived cells) for therapeutic angiogenesis.2 Initially, the favorable effects of blood flow recovery in ischemic tissue were believed to be from the incorporation of EPCs into endothelial cells,3 but additional studies have shown that EPCs mediate angiogenesis by paracrine effects.4,5 However, both the optimal definition and characterization of EPCs remain controversial. A number of factors have been shown to modulate the functions of EPCs.6,7