切换至 "中华医学电子期刊资源库"

中华消化病与影像杂志(电子版) ›› 2017, Vol. 07 ›› Issue (01) : 36 -40. doi: 10.3877/cma.j.issn.2095-2015.2017.01.008

所属专题: 文献

综述

糖基转移酶与炎症性肠病的研究进展
谢隆科1, 王志荣1,()   
  1. 1. 200065 上海,同济大学附属同济医院消化内科
  • 收稿日期:2016-05-10 出版日期:2017-02-01
  • 通信作者: 王志荣

Research progress of glycosyltransferase and inflammatory bowel disease

Longke Xie1, Zhirong Wang1,()   

  1. 1. Department of Gastroenterology, Tongji Hospital, Tongji University, Shanghai 20065, China
  • Received:2016-05-10 Published:2017-02-01
  • Corresponding author: Zhirong Wang
  • About author:
    Corresponding author: Wang Zhirong, Email:
引用本文:

谢隆科, 王志荣. 糖基转移酶与炎症性肠病的研究进展[J]. 中华消化病与影像杂志(电子版), 2017, 07(01): 36-40.

Longke Xie, Zhirong Wang. Research progress of glycosyltransferase and inflammatory bowel disease[J]. Chinese Journal of Digestion and Medical Imageology(Electronic Edition), 2017, 07(01): 36-40.

目前炎症性肠病主要认为与遗传、感染、环境和免疫因素等有关,其中黏膜免疫遗传在持续肠道炎症中起着重要作用。糖基转移酶是糖基化过程的关键酶。糖基转移酶所催化的糖基化产物在炎症反应、免疫系统、肿瘤转移以及细菌定植和感染等都有重要作用。糖基转移酶在炎症性肠病中作用机制尚未完全探明,本文将现有关于糖基转移酶与炎症性肠病的研究进行综述。目前发现,岩藻糖基转移酶2、岩藻糖基转移酶8、N-乙酰氨基葡萄糖转移酶V和core 1β1,3-半乳糖基转移酶特定的分子伴侣(C1GALT1C1)等在炎症性肠病发病机制中有重要作用。糖基化在蛋白翻译后修饰占有重要作用,因此我们相信糖基转移酶会是解开炎症性肠病的分子机制的重要一环。

Inflammatory bowel disease(IBD)is currently considered to be a complex disease which arises as a result of the interaction of genetic, infectious, environmental and immunological factors leading to inflammatory responses in the intestinal tract.Amongst these factors are the immunological and the genetic factors of the most importance.Glycosyltransferases(GTs)are key enzymes of glycosylation.The products catalyzed by GTs play a pivotal role in pathological processes including inflammatory response, immune system, tumor metastasis as well as bacterial colonization and infection, etc.However, the particular role of GTs in IBD remains unclear.In this paper, recent studies on the relationship between IBD and GTs will be reviewed.It has been proved so far that fucosyltransferase 2, alpha(1, 6)fucosyltransferase, N-acetylglucosaminyltransferase V(GnT-V)and core 1β1, 3-galactosyltransferase-specific chaperone 1(C1GALT1C1)are associated with IBD.Since glycosylation plays an important role in post-translational protein modification, we hypothesize then studies on GTs may uncover the etiological mechanism of IBD.

1
刘占举,冯百岁.我国炎症性肠病研究进展和挑战[J].中华消化杂志,2014,34(4):221-223.
2
Theodoratou E, Campbell H, Ventham NT, et al.The role of glycosylation in IBD[J]. Nat Rev Gastroenterol Hepatol, 2014, 11(10): 588-600.
3
Brockhausen I. Crossroads between bacterial and mammalian glycosyltransferases[J]. Front Immunol, 2014, 5: 492.
4
胡定元,邵晓晓,郑波,等.岩藻糖基转移酶2和3基因多态性与溃疡性结肠炎的关系[J].中华内科杂志,2013,52(12):1053-1055.
5
Rausch P, Rehman A, Kunzel S, et al.Colonic mucosa-associated microbiota is influenced by an interaction of Crohn disease and FUT2(Secretor)genotype[J]. Proc Natl Acad Sci U S A, 2011, 108(47): 19030-19035.
6
Wacklin P, Tuimala J, Nikkilä J, et al.Faecal Microbiota Composition in Adults Is Associated with the FUT2 Gene Determining the Secretor Status[J]. PLoS One, 2014, 9(4): e94863.
7
McGovern DP, Jones MR, Taylor KD, et al.Fucosyltransferase 2(FUT2)non-secretor status is associated with Crohn′s disease[J]. Hum Mol Genet, 2010, 19(17): 3468-3476.
8
Hu DY, Shao XX, Xu CL, et al.Associations of FUT2 and FUT3 gene polymorphisms with Crohn′s disease in Chinese patients[J]. J Gastroenterol Hepatol, 2014, 29(10): 1778-1785.
9
Aheman A, Luo HS, Gao F. Association of fucosyltransferase 2 gene variants with ulcerative colitis in Han and Uyghur patients in China[J]. World J Gastroenterol, 2012, 18(34): 4758-4764.
10
Parmar AS, Alakulppi N, Paavola-Sakki P, et al.Association study of FUT2(rs601338)with celiac disease and inflammatory bowel disease in the Finnish population[J]. Tissue Antigens, 2012, 80(6): 488-493.
11
Wang Y, Fukuda T, Isaji T, et al.Loss of a1, 6-fucosyltransferase inhibits chemical-induced hepatocellular carcinoma and tumorigenesis by down-regulating several cell signaling pathways[J]. FASEB J, 2015, 29(8): 3217-3227.
12
Muinelo-Romay L, Villar-Portela S, Cuevas Alvarez E, et al.α(1, 6)Fucosyltransferase expression is an independent prognostic factor for disease-free survival in colorectal carcinoma[J]. Human Pathology, 2011, 42(11): 1740-1750.
13
Lauc G, Huffman JE, Pučicć M, et al.Loci Associated with N-Glycosylation of Human Immunoglobulin G Show Pleiotropy with Autoimmune Diseases and Haematological Cancers[J]. PLoS Genet, 2013, 9(1): e1003225.
14
Fujii H, Shinzaki S, Iijima H, et al.Core Fucosylation on T Cells, Required for Activation of T-Cell Receptor Signaling and Induction of Colitis in Mice, Is Increased in Patients With Inflammatory Bowel Disease[J]. Gastroenterology, 2016, 150(7): 1620-1632.
15
Breton C, Mucha J, Jeanneau C. Structural and functional features of glycosyltransferases[J]. Biochimie, 2001, 83(8): 713-718.
16
Li D, Li Y, Wu X, et al.Knockdown of Mgat5 inhibits breast cancer cell growth with activation of CD4+T cells and macrophages[J]. J Immunol, 2008, 180(5): 3158-3165.
17
Terao M, Ishikawa A, Nakahara S, et al.Enhanced epithelialmesenchymaltransition-like phenotype in N-acetylglucosaminyltransferaseV transgenic mouse skin promotes woundhealing[J]. J Biol Chem, 2011, 286(32): 28303-28311.
18
Shinzaki S, Ishii M, Fujii H, et al.N-Acetylglucosaminyltransferase V exacerbates murine colitis with macrophage dysfunction and enhances colitic tumorigenesis[J]. J Gastroenterol, 2015, 51(4): 357-369.
19
Dias AM, Dourado J, Lago P, et al.Dysregulation of T cell receptor N-glycosylation: a molecular mechanism involved in ulcerative colitis[J]. Human Molecular Genetics, 2014, 23(9): 2416-2427.
20
Grigorian A, Lee SU, Tian W, et al.Control of T Cell-mediated autoimmunity by metabolite flux to N-glycan biosynthesis[J]. J Biol Chem, 2007, 282(27): 20027-20035.
21
Grigorian A, Araujo L, Naidu NN, et al.Naidu, et al.N-acetylglucosamine inhibits T-helper 1(Th1)/T-helper 17(Th17)cell responses and treats experimental autoimmune Encephalomyelitis[J]. J Biol Chem, 2011, 286(46): 40133-40141.
22
王晓龙,陈新涛,曲戈,等.M1型、M2型巨噬细胞及肿瘤相关巨噬细胞中miR-146a表达的差异[J].郑州大学学报:医学版,2015,50(2):225-228.
23
Zhu W, Yu J, Nie Y, et al.Disequilibrium of M1 and M2 macrophages correlates with the development of experimental inflammatory bowel diseases[J]. Immunol Invest, 2014, 43(7): 638-652.
24
Pelaseyed T, Bergström JH, Gustafsson JK, et al.The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system[J]. Immunol Rev, 2014, 260(1): 8-20.
25
Xia L, Ju T, Westmuckett A, et al.Defective angiogenesis and fatal embryonic hemorrhage in mice lacking core 1-derived O-glycans[J]. J Cell Biol, 2004, 164(3): 451-459.
26
Fu J, Wei B, Wen T, et al.Loss of intestinal core 1-derived O-glycans causes spontaneous colitis in mice[J]. J Clin Invest, 2011, 121(4): 1657-1666.
27
Chang D, Gao F, Slavney A, et al.Accounting for eXentricities: Analysis of the X Chromosome in GWAS Reveals XLinked Genes Implicated in Autoimmune Diseases[J]. PLoS One, 2014, 9(12): e113684.
[1] 李合, 周晓华, 陈兴超. 四十例术后炎性肠梗阻诊疗分析[J]. 中华普外科手术学杂志(电子版), 2021, 15(01): 101-103.
[2] 乔雨晴, 沈磊, 周林香, 李湘杰, 严博. 结缔组织生长因子单克隆抗体对小鼠慢性结肠炎肠壁纤维化的作用[J]. 中华结直肠疾病电子杂志, 2023, 12(02): 125-131.
[3] 江学良. 炎症性肠病非药物疗法的实践与展望[J]. 中华消化病与影像杂志(电子版), 2017, 07(01): 1-3.
阅读次数
全文


摘要