Immunology Laboratory, Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.
Cell Biol Int. 2012 Sep;36(9):793-801. doi: 10.1042/CBI20110595.
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.
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。