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首页> 外文期刊>Cell motility and the cytoskeleton >Thymosin beta10 inhibits cell migration and capillary-like tube formation of human coronary artery endothelial cells.
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Thymosin beta10 inhibits cell migration and capillary-like tube formation of human coronary artery endothelial cells.

机译：胸腺素beta10抑制人冠状动脉内皮细胞的细胞迁移和毛细管样管形成。

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摘要

Thymosin beta10 is a cytoplasm G-actin sequestering protein whose functions are largely unknown. To determine the direct effects of exogenous thymosin beta10 on angiogenic potentials as endothelial cell migration and capillary-like tube formation, human coronary artery endothelial cells (HCAECs) were incubated with increasing doses of thymosin beta10 (25-100 ng/ml). By using a modified Boyden chamber assay, thymosin beta10 inhibited cell migration in a dose- and time-dependent manner with the maximal effect being a 36% reduction at 100 ng/ml as compared to controls (P < 0.01). In addition, thymosin beta10 (100 ng/ml) significantly inhibited the capillary-like tube-formation of HCAECs on Matrigel, showing a 21% reduction of the total tube length as compared to negative controls (P < 0.01). Furthermore, by using real time PCR analysis, thymosin beta10 significantly decreased mRNA levels of vascular endothelial growth factor (VEGF), VEGF receptor-1 (VEGFR-1) and integrin alphaV after 24 h treatment in HCAECs. By contrast, thymosin beta4 significantly increased HCAEC migration. These results indicate that thymosin beta10, but not thymosin beta4, have direct inhibitive effects on endothelial migration and tube formation that might be mediated via downregulation of VEGF, VEGFR-1 and integrin alphaV in HCAECs. This study suggests a potential therapeutic application of thymosin beta10 to the diseases with excessive angiogenesis such as cancer.
机译：胸腺素β10是一种胞质G-肌动蛋白螯合蛋白，其功能尚不清楚。为了确定外源性胸腺素β10对血管内皮细胞迁移和毛细血管样血管形成的潜在直接作用，将人类冠状动脉内皮细胞（HCAEC）与剂量增加的胸腺素β10（25-100 ng / ml）进行孵育。通过使用改良的博登室试验，胸腺素β10以剂量和时间依赖性方式抑制细胞迁移，与对照组相比，最大作用是在100 ng / ml下降低了36％（P <0.01）。此外，胸腺素β10（100 ng / ml）显着抑制了Matrigel上HCAEC的毛细管样管形成，与阴性对照相比，总管长减少了21％（P <0.01）。此外，通过实时PCR分析，在HCAEC中治疗24小时后，胸腺素beta10显着降低了血管内皮生长因子（VEGF），VEGF受体1（VEGFR-1）和整联蛋白alphaV的mRNA水平。相比之下，胸腺素beta4显着增加了HCAEC迁移。这些结果表明，胸腺素β10，而不是胸腺素β4，对内皮细胞迁移和管形成具有直接抑制作用，这可能是由于HCAECs中VEGF，VEGFR-1和整联蛋白αV的下调介导的。这项研究表明胸腺素β10在具有过度血管生成的疾病（例如癌症）中的潜在治疗应用。

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