ELAM-1-依赖细胞对血管内皮的粘附,由一个转染的人类fucosyltransferasecDNA确定
J B Lowe1, L M Stoolman, R P Nair
1Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor 48109-0650.
Cell
|November 2, 1990
概括
特定的fucosyltransferases通过控制sialyl Lewis x表达来调节白细胞对内皮白细胞粘附分子-1 (ELAM-1) 的粘附. 这一发现阐明了炎症细胞粘附的关键机制.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 葡萄糖生物学 葡萄糖生物学
背景情况:
- 白细胞对血管内皮的粘附在炎症期间至关重要.
- 内皮白细胞粘附分子-1 (ELAM-1) 通过其碳水化合物识别域 (CRD) 调解这一过程.
- 此前,ELAM-1的CRD的确切作用及其对碳水化合物结合的特异性尚不清楚.
研究的目的:
- 研究ELAM-1的CRD对细胞粘附的贡献.
- 为了确定ELAM-1的碳水化合物结合特异性.
- 为了阐明fucosyltransferases在ELAM-1-中介粘附中的作用.
主要方法:
- 人类fucosyltransferasecDNA转移到非骨髓状细胞系.
- 评估ELAM-1-依赖的内皮粘附.
- 分析碳水化合物决定因素的细胞表面表达.
主要成果:
- 被转染的细胞表现出ELAM-1-依赖于内皮的粘附性.
- 粘附与sialyl Lewis x 四糖的 de novo 表达相关.
- 易斯X sialyl的生物合成与转移的fucosyltransferase活性直接相关.
结论:
- 特定的α(1,3) 基转移酶调节ELAM-1-介导的细胞粘附.
- 这些酶调节了sialyl Lewis x和相关结构的细胞表面表达.
- 易斯Sialyl x是炎症期间与ELAM-1结合的关键决定因素.
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