title: β-1,4-Galactosyltransferase I involved in Schwann cells proliferation and apoptosis induced by tumor necrosis factor-alpha via the activation of MAP kinases signal pathways.
abstract: β-1,4-galactosyltransferase-I (β-1,4-GalT-I) plays a critical role in the initiation and maintenance of peripheral nervous system inflammatory reaction. However, the exact function of β-1,4-GalT-I in the regulation of SCs proliferation and apoptosis remains unclear. In this study, we found that low concentration of tumor necrosis factor-alpha (TNF-α) induced SCs proliferation, while high concentration of TNF-α induced SCs apoptosis. Meanwhile, the expressions of β-1,4-GalT-I, TNFR1, and TNFR2 were changed following. When β-1,4-GalT I overexpression, low concentration of TNF-α-induced SCs proliferation was partially repressed. Concurrently, the activity of ERK1/2 was decreased. While knocking down β-1,4-GalT I expression, high concentration of TNF-α-induced SCs apoptosis was partially rescued. Consistent with this, the activity of P38 and JNK were decreased. We also found anti-TNFR2 antibody suppressed low concentration of TNF-α-induced SCs proliferation, while anti-TNFR1 antibody inhibited high concentration of TNF-α-induced SCs apoptosis. Thus, present data show that β-1,4-GalT I may play an important role in SCs proliferation and apoptosis induced by TNF-α via different signal pathways and TNFR.
authors.affiliation: Department of Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Yuan
authors.forename: Huiguang
authors.initials: H
authors.lastname: Yang
authors.forename: Chun
authors.initials: C
authors.lastname: Cheng
authors.forename: Chunmiao
authors.initials: C
authors.lastname: Li
authors.forename: Xiujie
authors.initials: X
authors.lastname: Wu
authors.forename: Weipeng
authors.initials: W
authors.lastname: Huan
authors.forename: Huiqing
authors.initials: H
authors.lastname: Sun
authors.forename: Zhengming
authors.initials: Z
authors.lastname: Zhou
authors.forename: Yingying
authors.initials: Y
authors.lastname: Wang
authors.forename: Yunhong
authors.initials: Y
authors.lastname: Zhao
authors.forename: Xiang
authors.initials: X
authors.lastname: Lu
authors.forename: Aiguo
authors.initials: A
authors.lastname: Shen
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation; D002478:Cells, Cultured; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D020935:MAP Kinase Signaling System; D009237:N-Acetyllactosamine Synthase / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000378:metabolism; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000378:metabolism; D012583:Schwann Cells / Q000201:enzymology / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; C506237:Tnfrsf1a protein, rat; D014409:Tumor Necrosis Factor-alpha; D009237:N-Acetyllactosamine Synthase; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; C505410:Casp3 protein, rat; D053148:Caspase 3