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人脐带血源间充质干细胞(hUCB-MSC)抑制 K562(人红白血病髓样细胞系)的增殖。

Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSC) inhibit the proliferation of K562 (human erythromyeloblastoid leukaemic cell line).

机构信息

Immunology Laboratory, Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.

出版信息

Cell Biol Int. 2012 Sep;36(9):793-801. doi: 10.1042/CBI20110595.

Abstract

hUCB-MSC (human umbilical cord blood-derived mesenchymal stem cells) offer an attractive alternative to bone marrow-derived 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 hUCB-MSC. 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. hUCB-MSC inhibited proliferation of K562, arresting them in the G0 /G1 phase. NO (nitric oxide) was not involved in the hUCB-MSC-mediated 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, IFNα (interferon α), 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-cultured with K562. The anti-proliferative effect of hUCB-MSC was due to arrest of the growth of K562 in the G0 /G1 phase. The mechanisms underlying increased IL-6 and IL-8 secretion and LAP (latency-associated peptide; TGFβ1) by hUCB-MSC remains unknown.

摘要

人脐带来源的间充质干细胞(hUCB-MSC)比骨髓来源的 MSC 更具侵袭性,是一种生物材料来源,因此为细胞治疗提供了一种有吸引力的替代方法。我们已经评估了 hUCB-MSC 对 K562(一种红白血病母细胞系)增殖的影响和 hUCB-MSC 的细胞因子分泌模式。hUCB-MSC 与 K562 共培养导致 K562 的增殖呈剂量依赖性抑制。然而,在 Transwell 中,抗增殖作用降低,表明直接细胞-细胞接触的重要性。hUCB-MSC 抑制 K562 的增殖,将其阻滞在 G0 / G1 期。NO(一氧化氮)不参与 hUCB-MSC 介导的肿瘤抑制。hUCB-MSC 条件培养基中存在明显的 IL-6(白细胞介素 6)和 IL-8,但在其他 29 种细胞因子中未发现明显增加。hUCB-MSC 不分泌 Th1 细胞因子 IFNα(干扰素 α)、Th2 细胞因子 IL-4 和 Th17 细胞因子 IL-17。与 K562 共培养的 hUCB-MSC 表达潜伏膜结合形式 TGFβ1 的数量增加。hUCB-MSC 的抗增殖作用是由于 K562 在 G0 / G1 期生长停滞。hUCB-MSC 增加 IL-6 和 IL-8 分泌和 LAP(潜伏相关肽;TGFβ1)的机制尚不清楚。

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