首页> 外文期刊>Cell biology international. >Human umbilical cord blood-derived mesenchymal stem cells (hucb-MSC) inhibit the proliferation of K562 (human erythromyeloblastoid leukaemic cell line)
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Human umbilical cord blood-derived mesenchymal stem cells (hucb-MSC) inhibit the proliferation of K562 (human erythromyeloblastoid leukaemic cell line)

机译:人脐带血间充质干细胞(hucb-MSC)抑制K562(人红细胞母细胞样白血病细胞系)的增殖

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摘要

hUCB-MSC (human umbilical cord blood-derived mesenchymal stem cells) offer an attractive alternative to bone marrowderived MSC for cell-based therapy by being less invasive a source of biological material. We have evaluated the effect of hUCB-MSC on the proliferation of K562 (an erythromyeloblastoid cell line) and the cytokine secretion pattern of hUCBMSC. Co-culturing of hUCB-MSC and K562 resulted in inhibition of proliferation of K562 in a dose-dependent manner. However, the anti-proliferative effect was reduced in transwells, suggesting the importance of direct cell-to-cell contact. hUCBMSC inhibited proliferation of K562, arresting them in the G 0/G 1 phase. NO (nitric oxide) was not involved in the hUCB-MSCmediated tumour suppression. The presence of IL-6 (interleukin 6) and IL-8 were obvious in the hUCB-MSC conditioned media, but no significant increase was found in 29 other cytokines. Th1 cytokines, IFNγ (interferon γ), Th2 cytokine IL-4 and Th17 cytokine, IL-17 were not secreted by hUCB-MSC. There was an increase in the number of hUCB-MSC expressing the latent membrane-bound form of TGFβ1 co-cul tured with K562. The ant i-proliferative ef fect of hUCB-MSC was due to arrest of the growth of K562 in the G 0/G 1 phase. The mechanisms underlying increased IL-6 and IL-8 secretion and LAP (latency-associated peptide; TGFβ1) by hUCB-MSC remains unknown.
机译:hUCB-MSC(人脐血来源的间充质干细胞)由于其侵入性较小,是生物材料的来源,因此可替代骨髓来源的MSC用于细胞治疗。我们已经评估了hUCB-MSC对K562(一种成红细胞系细胞系)增殖和hUCBMSC细胞因子分泌模式的影响。 hUCB-MSC和K562的共培养导致K562增殖的抑制呈剂量依赖性。然而,在transwells中抗增殖作用降低,表明直接的细胞间接触非常重要。 hUCBMSC抑制K562的增殖,将其阻滞在G 0 / G 1期。 NO(一氧化氮)不参与hUCB-MSC介导的肿瘤抑制。在hUCB-MSC条件培养基中,IL-6(白介素6)和IL-8的存在很明显,但在其他29种细胞因子中却没有发现显着增加。 hUCB-MSC不分泌Th1细胞因子IFNγ(干扰素γ),Th2细胞因子IL-4和Th17细胞因子IL-17。表达与K562共同培养的TGFβ1潜伏膜结合形式的hUCB-MSC数量增加。 hUCB-MSC的抗i增殖作用归因于K562在G 0 / G 1期的生长停滞。 hUCB-MSC引起IL-6和IL-8分泌增加以及LAP(潜伏期相关肽;TGFβ1)的潜在机制仍然未知。

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