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首页> 外文期刊>Life sciences >In vivo trafficking of endothelial progenitor cells their possible involvement in the tumor neovascularization.
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In vivo trafficking of endothelial progenitor cells their possible involvement in the tumor neovascularization.

机译：体内内皮祖细胞的运输可能参与了肿瘤新血管形成。

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Circulating endothelial progenitor cell (EPCs) have been reported to contribute to vasculogenesis in adult organisms. To investigate the possible recruitment of EPCs and organization to form tumor vasculature, we investigated the in vivo real-time trafficking of EPCs non-invasively by using positron emission tomography (PET). A conditionally immortalized endothelial cell line derived from rat bone marrow (TR-BME1) was labeled with [2-(18)F] 2-fluoro-2-deoxy-D-glucose (FDG) and chased the accumulation in the rat tumor with PET. TR-BME1 cells were accumulated in the tumor tissues time-dependently. To investigate that the accumulation of the cells is specific or not, rats were previously irradiated with gamma-ray to suppress the influence of non-labeled EPCs derived from its bone marrow and used for PET analysis. The accumulation of TR-BME1 cells in the tumor was enhanced in gamma-ray-irradiated rats compared with that of non-irradiated ones, suggesting that TR-BME1 cells accumulated in the tumor specifically like as EPCs. Then the involvement of matrix metalloproteinases (MMPs) in EPC recruitment was examined. An inhibitor of MMP, MMI270, which suppressed invasion and tube formation abilities of TR-BME1 cells, only slightly suppressed the accumulation of TR-BME1 cells in the tumor of rats. These results suggest that EPCs are recruited in the tumor tissues for formation of tumor vasculature, and demonstrate the usefulness of TR-BME1 cells for studies on EPC related phenomena.
机译：据报道，循环内皮祖细胞（EPC）有助于成年生物体内的血管生成。为了调查EPC的可能募集和组织形成肿瘤脉管系统，我们使用正电子发射断层扫描（PET）研究了EPC的体内实时无创交易。用[2-（18）F] 2-氟-2-脱氧-D-葡萄糖（FDG）标记源自大鼠骨髓的条件无限增殖的内皮细胞系（TR-BME1），并追逐其在大鼠肿瘤中的积累宠物。 TR-BME1细胞是时间依赖性地积累在肿瘤组织中的。为了研究细胞的蓄积是否具有特异性，预先对大鼠进行了伽玛射线照射以抑制源自其骨髓的未标记EPC的影响，并将其用于PET分析。与未照射的大鼠相比，在γ射线照射的大鼠中，TR-BME1细胞在肿瘤中的积累得以增强，这表明TR-BME1细胞像EPCs一样在肿瘤中积累。然后检查了基质金属蛋白酶（MMP）在EPC募集中的参与。 MMP抑制剂MMI270抑制了TR-BME1细胞的侵袭和管形成能力，仅轻微抑制了TR-BME1细胞在大鼠肿瘤中的蓄积。这些结果表明，EPC被募集到肿瘤组织中以形成肿瘤脉管系统，并且证明TR-BME1细胞对于研究EPC相关现象是有用的。

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