Katoh S, Miyagi T, Taniguchi H, Matsubara Y, Kadota J, Tominaga A, Kincade P W, Matsukura S, Kohno S
Third Department of Internal Medicine, Miyazaki Medical College, Japan.
J Immunol. 1999 May 1;162(9):5058-61.
Previous studies established that variable degrees and types of glycosylation can account for differences in the ability of CD44 to function as a receptor for hyaluronic acid. We have now used neuraminidase treatment to conclude that sialylation negatively regulates CD44 on the human monocytic cell line THP-1 and peripheral blood monocytes. Both of these cell types displayed increased receptor activity after overnight culture with LPS. Of particular interest, the sialidase inhibitor 2-deoxy-2, 3-dehydro-N-acetylneuraminic acid completely blocked the LPS induced recognition of hyaluronic acid by THP-1 cells. Furthermore, acquisition of this characteristic paralleled induction of one type of sialidase activity. Monocytes may be capable of enzymaticly remodeling cell surface CD44, altering their ability to interact with the extracellular matrix.
先前的研究表明,不同程度和类型的糖基化可解释CD44作为透明质酸受体功能能力的差异。我们现在使用神经氨酸酶处理得出结论,唾液酸化对人单核细胞系THP-1和外周血单核细胞上的CD44起负调节作用。这两种细胞类型在用LPS过夜培养后均表现出受体活性增加。特别有趣的是,唾液酸酶抑制剂2-脱氧-2,3-脱氢-N-乙酰神经氨酸完全阻断了LPS诱导的THP-1细胞对透明质酸的识别。此外,这种特性的获得与一种唾液酸酶活性的诱导平行。单核细胞可能能够通过酶促方式重塑细胞表面的CD44,改变其与细胞外基质相互作用的能力。