Decrease in cell surface sialic acid in etoposide-treated Jurkat cells and the role of cell surface sialidase
Decrease in cell surface sialic acid in etoposide-treated Jurkat cells and the role of cell surface sialidase
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DOI：
10.1023/a:1007165403771
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发表时间：
2000-05-01
影响因子：
3
通讯作者：
Matsumoto, K
中科院分区：
文献类型：
--
作者：
Azuma, Y;Taniguchi, A;Matsumoto, K
本研究通过用拓扑异构酶II抑制剂依托泊苷诱导细胞凋亡，探讨了Jurkat细胞表面糖链改变的潜在机制。在依托泊苷处理3小时内，流式细胞术分析显示，黑接骨木凝集素识别的α2,3 -连接唾液酸部分减少，蓖麻凝集素识别的半乳糖增加。结果表明，在依托泊苷处理的细胞表面，糖缀合物上的去唾液酸糖链迅速被诱导产生。为了阐明去唾液酸化机制，我们研究了依托泊苷诱导细胞凋亡过程中α2,3 -唾液酸转移酶mRNA的表达以及细胞表面唾液酸酶的活性。在依托泊苷处理2小时内，hST3Gal III和hST3Gal IV mRNAs的表达下调，细胞表面唾液酸酶活性增加了三倍。此外，在唾液酸酶抑制剂2,3 -脱氢 - 2 -脱氧 - N -乙酰神经氨酸存在的情况下，α2,3 -连接唾液酸水平的降低被显著抑制。这些结果表明，依托泊苷处理诱导了细胞表面唾液酸酶的激活或暴露，这是唾液酸减少的主要原因。
The present study investigated the mechanism underlying alterations of cell surface sugar chains of Jurkat cells by inducing apoptosis with etoposide, an inhibitor of topoisomerase II. Within 3 h of etoposide treatment, flowcytometric analysis revealed a decrease in Maackia amurensis agglutinin recognized alpha2,3-linked sialic acid moieties and an increase in Ricinus communis agglutinin recognized galactose. The results suggested that asialo-sugar chains on glycoconjugates were rapidly induced on the etoposide-treated cell surface. To clarify the desialylation mechanism, we studied alpha2,3-sialyltransferase mRNA expression and the activity of sialidase on the cell surface during etoposide-induced apoptosis. The expression of hST3Gal III and hST3Gal IV mRNAs were down-regulated and sialidase activity on the cell surface increased threefold within 2 h of etoposide treatment. Moreover, the decrease in alpha2,3-linked sialic acid levels was significantly suppressed in the presence of 2,3-dehydro-2-deoxy-N-acetylneuraminic acid, an inhibitor of sialidase. These results suggested that activation or exposure of sialidase on the cell surface was induced by etoposide treatment and was the main cause of the decrease in sialic acids.