Prostacyclin: a potential new target for endothelial progenitor cell-mediated angiogenesis.
Prostacyclin: a potential new target for endothelial progenitor cell-mediated angiogenesis.
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前列环素：内皮祖细胞介导的血管生成的潜在新靶点。
DOI：
10.1253/circj.cj-13-0143
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发表时间：
2013
影响因子：
3.3
通讯作者：
Uichi Ikeda
中科院分区：
文献类型：
--
作者：
Y. Shiba;Uichi Ikeda
PGI 2在EPC介导的血管生成中的作用尚不清楚。He等9表明，环氧合酶（考克斯）的酶活性和随后产生的PGI 2通过PPARδ途径增强EPC介导的血管生成。他们表明，EPCs中考克斯-1/PGI 2/PPARδ通路的激活导致EPCs通过PGI 2特异性受体IP独立、直接分化为内皮细胞。Kawabe等人表明，从EPC中去除IP会导致其功能障碍10，在该研究之后，包括Aburakawa等人在内的同一小组描述了PGI 2/IP信号在EPC介导的血管生成中的关键作用。11在本期杂志中，作者比较了骨髓和非骨髓组织中PGI 2/IP信号对后肢缺血血流恢复的影响，使用遗传性IP缺陷小鼠的骨髓移植模型。他们观察到，与后肢缺血模型中的野生型小鼠相比，IP缺陷小鼠在接受野生型细胞的骨髓移植后，最初表现出血流量减少;在诱导后肢缺血的30天内，血流量减少完全恢复。相比之下，因斯Asahara等人在1997年发现内皮祖细胞（EPCs）1以来，已经进行了广泛的研究，不仅试图澄清和表征这些细胞，而且还试图利用含有EPCs的产物（即骨髓来源的细胞）用于治疗性血管生成。2最初，缺血组织中血流恢复的有利效果被认为是由于EPC掺入内皮细胞，3但其他研究表明，EPCs通过旁分泌效应介导血管生成。4，5然而，EPCs的最佳定义和表征仍存在争议。已证明有许多因素可调节EPC的功能。
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