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首页> 美国卫生研究院文献>Journal of the Boston Society of Medical Sciences >Increased Tie2 Expression Enhanced Response to Angiopoietin-1 and Dysregulated Angiopoietin-2 Expression in Hemangioma-Derived Endothelial Cells
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Increased Tie2 Expression Enhanced Response to Angiopoietin-1 and Dysregulated Angiopoietin-2 Expression in Hemangioma-Derived Endothelial Cells

机译：在血管瘤来源的内皮细胞中增加Tie2表达增强对血管生成素1的反应以及血管生成素2的表达失调。

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Infantile hemangiomas are endothelial tumors that grow rapidly in the first year of life and regress slowly during early childhood. Although hemangiomas are well-known vascular lesions, little is known about the mechanisms that cause the excessive endothelial cell proliferation in these most common tumors of infancy. To investigate the molecular basis of hemangioma, we isolated endothelial cells from several proliferative-phase lesions and showed that these cells are clonal and exhibit abnormal properties in vitro (E. Boye, Y. Yu, G. Paranya, J. B. Mulliken, B. R. Olsen, J. Bischoff: Clonality and altered behavior of endothelial cells from hemangiomas. J Clin Invest 2001, 107:745–752). Here, we analyzed mRNA expression patterns of genes required for angiogenesis, including members of the vascular endothelial growth factor (VEGF)/VEGF receptor family and the angiopoietin/Tie family, in hemangioma-derived and normal endothelial cells. KDR, Flt-1, Tie1, Tie2, and angiopoietin-2 (Ang2) were strongly expressed in cultured hemangioma-derived endothelial cells and in hemangioma tissue. In contrast, there was little expression of angiopoietin-1 (Ang1) or VEGF. We found Tie2 mRNA and protein up-regulated with a concomitant increase in cellular responsiveness to Ang1 in most hemangioma-derived endothelial cells. Ang2 mRNA was down-regulated in response to serum in hemangioma-derived endothelial cells, but not in normal endothelial cells, suggesting altered regulation. These findings implicate Tie2 and its ligands Ang1 and Ang2 in the pathogenesis of hemangioma.
机译：小儿血管瘤是一种内皮肿瘤，在生命的第一年迅速生长，而在儿童早期则缓慢消退。尽管血管瘤是众所周知的血管病变，但对于这些最常见的婴儿肿瘤中导致内皮细胞过度增殖的机制了解甚少。为了研究血管瘤的分子基础，我们从几个增殖期病变中分离出内皮细胞，并显示这些细胞是克隆性的，并在体外表现出异常特性（E. Boye，Y. Yu，G. Paranya，JB Mulliken，BR Olsen， J. Bischoff：血管瘤的内皮细胞的克隆性和行为改变（J Clin Invest 2001，107：745-752）。在这里，我们分析了血管瘤来源的和正常的内皮细胞中血管生成所需基因的mRNA表达模式，包括血管内皮生长因子（VEGF）/ VEGF受体家族成员和血管生成素/ Tie家族成员。 KDR，Flt-1，Tie1，Tie2和血管生成素2（Ang2）在培养的血管瘤来源的内皮细胞和血管瘤组织中强烈表达。相比之下，血管生成素-1（Ang1）或VEGF的表达很少。我们发现在大多数血管瘤来源的内皮细胞中，Tie2 mRNA和蛋白上调同时伴随着对Ang1的细胞反应性的增加。 Ang2 mRNA在血管瘤来源的内皮细胞中响应血清而下调，但在正常内皮细胞中不下降，表明调节改变。这些发现暗示Tie2及其配体Ang1和Ang2在血管瘤的发病机理中。

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