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大鼠坐骨神经挤压伤后β-1,4半乳糖基转移酶I、V mRNA及Galβ1,4GlcNAc基团的表达变化

Expression change of beta-1,4 galactosyltransferase I, V mRNAs and Galbeta1,4GlcNAc group in rat sciatic nerve after crush.

作者信息

Yan Meijuan, Cheng Chun, Shao Xiaoyi, Qian Ji, Shen Aiguo, Xia Chunlin

机构信息

Laboratory of Aging and Nervous Diseases & Cytoneurobiology Unit, Soochow University, Suzhou, 215123, PR China.

出版信息

J Mol Histol. 2008 Jun;39(3):317-28. doi: 10.1007/s10735-008-9168-z. Epub 2008 Mar 5.

DOI:10.1007/s10735-008-9168-z
PMID:18320333
Abstract

Glycosylation is one of the most important post-translational modifications. It is clear that the single step of beta-1,4-galactosylation is performed by a family of beta-1,4-galactosyltransferases (beta-1,4-GalTs), and that each member of this family may play a distinct role in different tissues and cells. beta-1,4-GalT I and V are involved in the biosynthesis of N-linked oligosaccharides. In the present study, Real-time PCR revealed that the beta-1,4-GalT I and V mRNAs reached peaks at 2 w after sciatic nerve crush. In situ hybridization showed that at 1 d after sciatic nerve crush, the expression levels of beta-1,4-GalT I and V mRNAs were strong at the crush site, and decreased gradually from crush site to the distal segments. In addition, combined in situ hybridization for beta1,4-GalT I and V mRNAs and immunohistochemistry for S100 showed that beta1,4-GalT I and V mRNAs were mainly located in Schwann cells. Lectin blot showed that the expression of Galbeta1,4GlcNAc group increased at 6 h immediately, reached a peak at 12 h and remained elevated up to 4 w after sciatic nerve crush. In conclusion, beta1,4-GalT I and V might play important roles in the regeneration of the injured sciatic nerve, and upregulation of Galbeta1,4GlcNAc group might be correlated with the process of the sciatic nerve injury.

摘要

糖基化是最重要的翻译后修饰之一。很明显,β-1,4-半乳糖基化的单个步骤是由β-1,4-半乳糖基转移酶(β-1,4-GalTs)家族执行的,并且该家族的每个成员可能在不同组织和细胞中发挥不同作用。β-1,4-GalT I和V参与N-连接寡糖的生物合成。在本研究中,实时PCR显示坐骨神经挤压后2周β-1,4-GalT I和V的mRNA达到峰值。原位杂交显示坐骨神经挤压后1天,β-1,4-GalT I和V的mRNA在挤压部位表达水平很强,并从挤压部位向远端逐渐降低。此外,β1,4-GalT I和V的mRNA原位杂交与S100免疫组化相结合显示,β1,4-GalT I和V的mRNA主要位于雪旺细胞中。凝集素印迹显示,Galβ1,4GlcNAc基团的表达在坐骨神经挤压后6小时立即增加,在12小时达到峰值,并在4周内一直保持升高。总之,β1,4-GalT I和V可能在坐骨神经损伤的再生中发挥重要作用,Galβ1,4GlcNAc基团的上调可能与坐骨神经损伤过程相关。

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本文引用的文献

1
Peripheral regeneration.外周再生
Annu Rev Neurosci. 2007;30:209-33. doi: 10.1146/annurev.neuro.30.051606.094337.
2
Increased gene expression of beta-1,4-galactosyltransferase I in rat injured sciatic nerve.大鼠坐骨神经损伤后β-1,4-半乳糖基转移酶I基因表达增加。
J Mol Neurosci. 2003;21(2):103-10. doi: 10.1385/JMN:21:2:103.
3
Overexpression of beta-1,4-galactosyltransferase I in rat Schwann cells promotes the growth of co-cultured dorsal root ganglia.
Neurosci Lett. 2003 May 22;342(3):159-62. doi: 10.1016/s0304-3940(03)00271-4.
大鼠坐骨神经损伤后 Gem 的表达增加。
J Mol Histol. 2013 Feb;44(1):27-36. doi: 10.1007/s10735-012-9459-2. Epub 2012 Oct 18.
4
The neuroprotective effect of pyrroloquinoline quinone on traumatic brain injury.吡咯并喹啉醌对创伤性脑损伤的神经保护作用。
J Neurotrauma. 2012 Mar 20;29(5):851-64. doi: 10.1089/neu.2011.1882. Epub 2011 Dec 20.
5
β-1,4-Galactosyltransferase-involved in lipopolysaccharide-induced adhesion of Schwann cells.β-1,4-半乳糖基转移酶参与脂多糖诱导的雪旺细胞黏附。
Inflamm Res. 2011 Feb;60(2):169-74. doi: 10.1007/s00011-010-0251-z. Epub 2010 Oct 21.
6
Lipopolysaccharide induced upregulation of beta-1,4-galactosyltransferase-I in Schwann cell.脂多糖诱导施万细胞中β-1,4-半乳糖基转移酶-I 的上调。
Inflammation. 2009 Oct;32(5):279-86. doi: 10.1007/s10753-009-9131-5.
4
Targeted mutations in beta1,4-galactosyltransferase I reveal its multiple cellular functions.β1,4-半乳糖基转移酶I的靶向突变揭示了其多种细胞功能。
Biochim Biophys Acta. 2002 Dec 19;1573(3):258-70. doi: 10.1016/s0304-4165(02)00392-6.
5
Expression of beta-1,4-galactosyltransferase II and V in rat injured sciatic nerves.β-1,4-半乳糖基转移酶II和V在大鼠坐骨神经损伤中的表达
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6
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7
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9
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10
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