Murine 5T multiple myeloma cells induce angiogenesis in vitro and in vivo.

Murine 5T multiple myeloma cells induce angiogenesis in vitro and in vivo.
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DOI:
10.1038/sj.bjc.6600137
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发表时间:
2002-03-04
影响因子:
8.8
通讯作者:
Vanderkerken, K
Vanderkerken, K
中科院分区:
医学1区
文献类型:
--
作者:
Van Valckenborgh, E;De Raeve, H;Devy, L;Blacher, S;Munaut, C;Noel, A;Van Marck, E;Van Riet, I;Van Camp, B;Vanderkerken, K

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多发性骨髓瘤是B细胞恶性肿瘤。最近,研究表明多发性骨髓瘤患者的骨髓样本显示血管生成增强。所涉及的机制似乎是多重而复杂的。我们在此通过大鼠主动脉环实验证明小鼠5T多发性骨髓瘤模型能够在体外诱导血管生成,并通过测定微血管密度在体内诱导血管生成。在5T多发性骨髓瘤条件培养基中培养的大鼠主动脉环比在对照培养基中培养的大鼠主动脉环显示出更多的长微血管和更多的分支血管。在5T多发性骨髓瘤患病小鼠的骨髓样本中,与年龄匹配的对照组骨髓样本相比,微血管密度有统计学意义的增加。两种5T多发性骨髓瘤细胞的血管生成表型可能与它们产生血管内皮生长因子的能力有关,至少部分相关。这些数据清楚地表明,5T多发性骨髓瘤模型是研究多发性骨髓瘤血管生成的良好模型,将有助于揭示新生血管形成的机制,并测试新的推定血管生成抑制剂。英国癌症杂志(2002)86,796-802。DOI: 10.1038/sj/bjc/6600137 www.bjcancer.com©2002英国癌症研究中心
Multiple myeloma is a B cell malignancy. Recently, it has been demonstrated that bone marrow samples of patients with multiple myeloma display an enhanced angiogenesis. The mechanisms involved seem to be multiple and complex. We here demonstrate that the murine 5T multiple myeloma models are able to induce angiogenesis in vitro by using a rat aortic ring assay and in vivo by determining the microvessel density. The rat aortic rings cultured in 5T multiple myeloma conditioned medium exhibit a higher number of longer and more branched microvessels than the rings cultured in control medium. In bone marrow samples from 5T multiple myeloma diseased mice, a statistically significant increase of the microvessel density was observed when compared to bone marrow samples from age-matched controls. The angiogenic phenotype of both 5T multiple myeloma cells could be related, at least in part, to their capacity to produce vascular endothelial growth factor. These data clearly demonstrate that the 5T multiple myeloma models are good models to study angiogenesis in multiple myeloma and will allow to unravel the mechanisms of neovascularisation, as well as to test new putative inhibitors of angiogenesis. British Journal of Cancer (2002) 86, 796–802. DOI: 10.1038/sj/bjc/6600137 www.bjcancer.com © 2002 Cancer Research UK