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首页> 外文期刊>Advances in hematology >Does Adiponectin Act as an Antiangiogenic Factor in B-Cell Chronic Lymphocytic Leukemia?
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Does Adiponectin Act as an Antiangiogenic Factor in B-Cell Chronic Lymphocytic Leukemia?

机译:脂联素是否可作为B细胞慢性淋巴细胞白血病的抗血管生成因子?

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摘要

Angiogenesis is involved in the pathogenesis of B-cell chronic lymphocytic leukemia (CLL), and high microvascular density has been found in CLL to be associated with a poor prognosis. In this study, we assessed serum levels of adiponectin in 69 patients with Binet stage A B-CLL, and these values were retrospectively correlated with bone marrow (BM) microvessel area and serum levels of vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), angiogenin, PECAM-1 (CD31), matrix metalloproteinase-9 (MMP-9), interleukin-8 (IL-8), syndecan-1, and the percentage ofCD38+orZAP-70+CLL cells. The positive correlation between serum levels of adiponectin and VEGF (P=.03) does not translate into an increase of the extent of BM angiogenesis (P=.404), FGF-2 (P=.348), angiogenin (P=.402), and CD31 (P=.248) serum concentrations. Accordingly, IL-8 (P=.175), syndecan-1 (P=.06), and MMP-9 (P=.144) circulating levels were not likely to reflect adiponectin concentration. Furthermore, patients with higher levels of adiponectin had a more favorable biological profile as defined by a lower number of bothCD38−(r=−0.294;P=.02) andZAP-70+(r=−0.285;P=.04). Finally, we evaluated the presence of adiponectin in B-CLL cells at gene expression level. RMA intensity values for adiponectin gene transcript denote a homogeneous low expression in B-CLL cells, whereas VEGF transcript was highly expressed with a degree of interpatient variability. Overall, these data seem to indicate that adiponectin could be involved as an antiangiogenic factor in B-CLL.
机译:血管生成与B细胞慢性淋巴细胞性白血病(CLL)的发病机理有关,并且在CLL中发现高微血管密度与不良预后相关。在这项研究中,我们评估了69例Binet A B-CLL患者的血清脂联素水平,并将这些值与骨髓(BM)微血管面积以及血管内皮生长因子(VEGF),成纤维细胞生长因子的血清水平相关联。 -2(FGF-2),血管生成素,PECAM-1(CD31),基质金属蛋白酶9(MMP-9),白介素8(IL-8),syndecan-1以及CD38 +或ZAP-70 + CLL的百分比细胞。血清脂联素和VEGF水平之间的正相关(P = .03)并不表示BM血管生成(P = .404),FGF-2(P = .348),血管生成素(P =。 402)和CD31(P = .248)血清浓度。因此,IL-8(P = .175),syndecan-1(P = .06)和MMP-9(P = .144)循环水平不太可能反映脂联素的浓度。此外,脂联素水平较高的患者具有更佳的生物学特征,这由较低的CD38-(r = -0.294; P = .02)和ZAP-70 +(r = -0.285; P = .04)定义。最后,我们在基因表达水平评估了B-CLL细胞中脂联素的存在。脂联素基因转录本的RMA强度值表示在B-CLL细胞中均一的低表达,而VEGF转录本则在患者之间具有一定程度的高度表达。总体而言,这些数据似乎表明脂联素可能是B-CLL的抗血管生成因子。

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