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CUTTING EDGE |
*
Third Department of Internal Medicine, Miyazaki Medical College, Miyazaki, Japan;
Division of Biochemistry, Research Institute, Miyagi Prefectural Cancer Center, Miyagi, Japan;
Second Department of Internal Medicine, Nagasaki University, School of Medicine, Nagasaki, Japan;
§
Department of Medical Biology, Kochi Medical School, Kochi, Japan; and
¶
Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104
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.
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