title: Elevated beta1,4-galactosyltransferase-I induced by the intraspinal injection of lipopolysaccharide.
abstract: Beta1,4-galactosyltransferase-I (beta1,4-GalT-I) is one of the best studied glycosyltransferases. Previous studies demonstrated that beta1,4-GalT-I was a major galactosyltransferase responsible for selectin-ligand biosynthesis and that inflammatory responses of beta1,4-GalT-I deficient mice were impaired. In this study, we investigate the expression of beta1,4-GalT-I in lipopolysaccharide (LPS)-induced neuroinflammatory processes. The results of this study demonstrated that beta1,4-GalT-I was strongly induced by intraspinal administration of LPS. More than 90% galactose-containing glycans and beta1,4-GalT-I were expressed in immune cells. The ELISA assay shows focal injection LPS also induces TNF-alpha alteration. Double staining indicated beta1,4-GalT-I overlapped with TNF-alpha. Moreover, RT-PCR for beta1,4-GalT-I mRNA showed that beta1,4-GalT-I mRNA in microglia in vitro was affected in a dose- and time dependent manner in response to LPS or TNF-alpha stimulation. All these results indicated that the increase of beta1,4-GalT-I might attribute to the effect of TNF-alpha excreting during inflammation. E-selectin, which ligand was modified by beta1,4-GalT-I, was correlated with galactose-containing glycans following injecting LPS into spinal cord. We therefore suggest that beta1,4-GalT-I may play an important role in regulating immune cell migration into the inflammatory site.
authors.affiliation: The Jiangsu Province Key Lab of Neuroregeneration, Nantong University, Nantong 226001, People's Republic of China.
authors.forename: Aiguo
authors.initials: A
authors.lastname: Shen
authors.forename: Jianping
authors.initials: J
authors.lastname: Chen
authors.forename: Ji
authors.initials: J
authors.lastname: Qian
authors.forename: Jianchun
authors.initials: J
authors.lastname: Zhu
authors.forename: Ling
authors.initials: L
authors.lastname: Hu
authors.forename: Meijuan
authors.initials: M
authors.lastname: Yan
authors.forename: Dan
authors.initials: D
authors.lastname: Zhou
authors.forename: Ying
authors.initials: Y
authors.lastname: Gao
authors.forename: Junling
authors.initials: J
authors.lastname: Yang
authors.forename: Fei
authors.initials: F
authors.lastname: Ding
authors.forename: Chun
authors.initials: C
authors.lastname: Cheng
mesh_terms: D000818:Animals; D002465:Cell Movement / Q000187:drug effects / Q000276:immunology; D019040:E-Selectin / Q000276:immunology / Q000378:metabolism; D004790:Enzyme Induction / Q000187:drug effects / Q000276:immunology; D005700:Galactosyltransferases / Q000096:biosynthesis* / Q000276:immunology; D007249:Inflammation / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051379:Mice; D009187:Myelitis / Q000139:chemically induced / Q000201:enzymology* / Q000276:immunology / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D019040:E-Selectin; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D005700:Galactosyltransferases