Modulation of K562 cells with sodium butyrate. Association of impaired NK susceptibility with sialic acid and analysis of other parameters
Modulation of K562 cells with sodium butyrate. Association of impaired NK susceptibility with sialic acid and analysis of other parameters
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用丁酸钠调节 K562 细胞。
DOI：
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发表时间：
1983
影响因子：
6.4
通讯作者：
J. Roder
中科院分区：
文献类型：
--
作者：
J. Werkmeister;H. Pross;J. Roder
神经氨酸酶处理亲本和丁酸诱导的 K562 肿瘤细胞与这些靶细胞自然杀伤 (NK) 敏感性的增加有关。对于 NK 抗性 (NRR) 丁酸盐分化的 K562 细胞，神经氨酸酶的增强程度显着更大，因此亲本 NK 敏感 (NKS) K562 系与其诱导的 NKR 变体在 NK 敏感性方面的相对差异不再是五倍或六倍，而是仅为两倍。神经氨酸酶处理后靶细胞 NK 敏感性改变的主要原因是这些细胞的靶细胞结合能力增加，这是通过使用 Percoll 富集 NK 细胞的直接缀合物形成细胞测定和冷靶竞争测定进行评估的。这种增强似乎不仅仅是由于细胞表面净负电荷减少而导致膜间吸引力增加，因为硫酸鱼精蛋白（一种带正电的分子）对 NK 活性没有影响。与 NKS 亲本 K562 肿瘤细胞相比，NKR 丁酸诱导的细胞具有高 3.6 至 4.0 倍的唾液酸转移酶活性，并且与在唾液酸糖蛋白（高 2.2 至 2.9 倍）和特别是神经节苷脂提取物（高 6.2 至 13.6 倍）中检测到的细胞表面唾液酸含量显着相关。与 NK 介导的丁酸盐诱导靶标细胞溶解作用的神经氨酸酶显着增强相一致，与 NKS 亲代 K562 细胞系相比，这些 NKR 细胞与神经氨酸酶可及的唾液酸水平显着增强相关。其他参数，如对超氧自由基的敏感性、内在超氧化物歧化酶水平、改变的膜修复机制和转铁蛋白竞争，在 NKS 和 NKR 靶表型之间没有显着差异。糖抑制研究表明，各种中性糖对丁酸盐诱导的细胞具有增强的抑制作用。磷酸化糖的抑制程度在亲本和诱导的 K562 肿瘤靶细胞之间具有可比性，并且与我们之前的研究结果一致，表明这些磷酸己糖可能以独立于靶细胞识别的步骤抑制细胞溶解。
Neuraminidase treatment of parental and butyrate‐induced K562 tumor cells was associated with an increase in natural killer (NK) susceptibility of these target cells. The degree of enhancement with neuraminidase was significantly greater for the NK‐resistant (NRR) butyrate‐differentiated K562 cells so that the relative difference between the parental NK‐sensitive (NKS) K562 line and its induced NKR variants, in terms of NK sensitivity, was no longer five‐ or six‐fold but only two‐fold. The predominant reason for the altered NK susceptibilities of the target cells after neuraminidase treatment was an increase in the target‐cell‐binding ability of these cells as assessed by a direct conjugate‐forming cell assay using Percoll‐enriched NK cells and cold target competition assays. The enhancement did not appear to be due simply to an increased membrane‐membrane attraction caused by a reduction of net negative cell surface charges since protamine sulphate, a positively charged molecule, had no effect on NK activity. Compared with the NKS parental K562 tumor cells, the NKR butyrate‐induced cells had 3.6‐to 4.0‐fold higher sialo‐transferase activities and were associated with significantly greater amounts of cell surface sialic acid detected both in sialyl glycoproteins (2.2‐ to 2.9‐fold higher) and particularly within ganglioside extracts (6.2‐ to 13.6‐fold higher). In conformity with the marked neuraminidase enhancement of NK‐mediated cytolysis of the butyrate‐induced targets, these NKR cells were associated with significantly enhanced levels of neuraminidase‐accessible sialic acid compared to the NKS parental K562 cell line. Other parameters such as sensitivity to superoxide radicals, intrinsic superoxide dismutase levels, altered membrane repair mechanisms and transferrin competition, were not significantly different between the NKS and NKR target phenotypes. Sugar inhibition studies demonstrated an enhanced inhibition against the butyrate‐induced cells with a variety of neutral sugars. The degree of inhibition with phosphorylated sugars was comparable between the parental and induced K562 tumor target cells and is consistent with our previous findings showing that these hexose phosphates may be inhibiting cytolysis at a step independent of target‐cell recognition.
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DOI：
--
发表时间：
1981
期刊：
Journal of immunology (Baltimore, Md. : 1950)
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DOI：
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发表时间：
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期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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