title: β-1,4-galactosyltransferase I promotes tumor necrosis factor-α autocrine via the activation of MAP kinase signal pathways in Schwann cells.
abstract: Recent studies have demonstrated that aberrant galactosylation is associated with some inflammation diseases. β-1,4-Galactosyltransferase-I (β-1,4-GalT I), which transferred galactose to the terminal N-acetylglucosamine of N- and O-linked glycans in a β-1,4-linkage, was considered to be the major galactosyltransferase among the seven members of the subfamily responsible for β4 galactosylation. To elucidate the expression and possible function of β-1,4-GalT I in the peripheral nervous system (PNS) inflammatory diseases, we performed a tumor necrosis factor-alpha (TNF-α) autocrine inflammatory model in Schwann cells (SCs). In this study, we found that silencing of β-1,4-GalT I suppressed TNF-α autocrine, while overexpression of β-1,4-GalT I promoted TNF-α autocrine in TNF-α-treated SCs. Meanwhile, anti-TNFR1 antibody suppressed the expression of β-1,4-GalT I, and TNF-α autocrine. β-1,4-GalT I conferred its effect by promoting ERK, JNK, and P38 MAP kinase signal pathways activation in TNF-α-induced SCs. Thus, the present data shows that during SCs activation, β-1,4-GalT I may play an important role in the release of inflammatory mediators.
authors: Department of Osteology, Affiliated Jiangyin Hospital of Nantong University, Medical Colledge, Nantong University, Nantong 226001 Jiangsu, People's Republic of China.
authors: Huiguang
authors: H
authors: Yang
authors: Qin
authors: Q
authors: Yuan
authors: Qian
authors: Q
authors: Chen
authors: Chunmiao
authors: C
authors: Li
authors: Xiujie
authors: X
authors: Wu
authors: Chen
authors: C
authors: Peng
authors: Lihua
authors: L
authors: Kang
authors: Xiang
authors: X
authors: Lu
authors: Huiqing
authors: H
authors: Sun
authors: Zhengming
authors: Z
authors: Zhou
authors: Aiguo
authors: A
authors: Shen
authors: Chun
authors: C
authors: Cheng
mesh_terms: D000818:Animals; D019898:Autocrine Communication / Q000502:physiology*; D004789:Enzyme Activation; D005700:Galactosyltransferases / Q000235:genetics / Q000378:metabolism*; D020868:Gene Silencing; D020935:MAP Kinase Signaling System / Q000502:physiology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000378:metabolism; D012583:Schwann Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism* / Q000494:pharmacology
chemical_list: D034741:RNA, Small Interfering; D047888:Receptors, Tumor Necrosis Factor, Type I; C506237:Tnfrsf1a protein, rat; D014409:Tumor Necrosis Factor-alpha; D005700:Galactosyltransferases; C119701:beta-1,4-galactosyltransferase I; D020928:Mitogen-Activated Protein Kinases