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Genetic variation and expression levels of tight junction genes identifies association between MAGI3 and inflammatory bowel disease
Karolinska Institute, Sweden; Regional Jonköping County, Sweden.
Karolinska Institute, Sweden; Karolinska University Hospital, Sweden.
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Regional Jonköping County, Sweden.
2017 (English)In: BMC Gastroenterology, ISSN 1471-230X, E-ISSN 1471-230X, Vol. 17, 68Article in journal (Refereed) Published
Abstract [en]

Background: Inflammatory bowel disease (IBD) is associated with increased intestinal permeability, which involves paracellular passage regulated through tight junctions (TJ). The aim of the study was to investigate single nucleotide polymorphisms (SNP) located in genes encoding interacting TJ proteins and corresponding expressions, in relation to IBD. Methods: Allelic associations between TJ-related genes (F11R, MAGI1, MAGI2, MAGI3, PARD3, PTEN, and TJP1) and IBD, Crohns disease (CD), or ulcerative colitis (UC) were investigated. PTPN22 was included since its located in the same genetic region as MAGI3. Gene expression levels were investigated in relation to genotype, inflammatory status, phenotype, and medical treatment. Results: The two strongest allelic associations were observed between IBD and SNPs in MAGI2 (rs6962966) and MAGI3 (rs1343126). Another MAGI3 SNP marker (rs6689879) contributed to increased ileal MAGI3 expression level in non-IBD controls. Furthermore, association between inflammation and decreased expression levels of MAGI3, PTEN, and TJP1 in colonic IBD as well as UC mucosa, and between inflammation and increased expression of PTPN22 in colonic IBD mucosa, was observed. Conclusions: Our findings lend support to a genetic basis for modulation of intestinal epithelial barrier in IBD, and we have identified MAGI3 as a new candidate gene for IBD.

Place, publisher, year, edition, pages
BIOMED CENTRAL LTD , 2017. Vol. 17, 68
Keyword [en]
Inflammatory bowel disease; Tight junctions; Single nucleotide polymorphism; Genetic predisposition; Gene expression
National Category
Gastroenterology and Hepatology
Identifiers
URN: urn:nbn:se:liu:diva-138239DOI: 10.1186/s12876-017-0620-yISI: 000402159500001PubMedID: 28545409OAI: oai:DiVA.org:liu-138239DiVA: diva2:1109387
Note

Funding Agencies|FORSS; Medical Research Council of South-Eastern Sweden [236541-2012, 235131-2012]; Futurum the Academy for Healthcare, Region Jonkoping County [FUTURUM-338631]; Bengt Ihre-Fonden [2012-SLS 254491]; Karolinska Institutets Forskningsfonder [2014fobi42063]

Available from: 2017-06-14 Created: 2017-06-14 Last updated: 2017-06-14

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