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Published on: January 30, 2014
beta-1,4-Galactosyltransferase-I participates in lipopolysaccharide induced reactive microgliosis
Jianping Chen1, HuiMin Wang, Huiguang Yang
1Laboratory Medicine Center, Affiliated Hospital of Nantong University, The Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, People's Republic of China.
beta-1,4-Galactosyltransferase-I (beta-1,4-GalT-I) is one of the best studied glycosyltransferases. Previous studies demonstrated that beta-1,4-GalT-I was a major galactosyltransferase responsible for selectin-ligand biosynthesis and that inflammatory responses of beta-1,4-GalT-I deficient mice were impaired. Our previous study suggest that beta-1,4-GalT-I may play an important role in regulating immune cell migration into the inflammatory site. In this study, we investigate beta-1,4-GalT-I may play an important role in mediating microgliosis. The results of this study demonstrated that beta-1,4-GalT-I was strongly induced in the ventral midbrain by intranigral injection of LPS. Most galactose-containing glycans and beta-1,4-GalT-I were expressed in microglia. Moreover, an Ab against beta-1,4-GalT-I attenuated both LPS-induced microglial activation and phagocytosis. We therefore suggest that beta-1,4-GalT-I may play an important role in regulating immune cell migration into the inflammatory site and mediating microgliosis.
beta-1,4-Galactosyltransferase-I (beta-1,4-GalT-I) is one of the best studied glycosyltransferases. Previous studies demonstrated that beta-1,4-GalT-I was a major galactosyltransferase responsible for selectin-ligand biosynthesis and that inflammatory responses of beta-1,4-GalT-I deficient mice were impaired. Our previous study suggest that beta-1,4-GalT-I may play an important role in regulating immune cell migration into the inflammatory site. In this study, we investigate beta-1,4-GalT-I may play an important role in mediating microgliosis. The results of this study demonstrated that beta-1,4-GalT-I was strongly induced in the ventral midbrain by intranigral injection of LPS. Most galactose-containing glycans and beta-1,4-GalT-I were expressed in microglia. Moreover, an Ab against beta-1,4-GalT-I attenuated both LPS-induced microglial activation and phagocytosis. We therefore suggest that beta-1,4-GalT-I may play an important role in regulating immune cell migration into the inflammatory site and mediating microgliosis.
