Genetic Analysis of Ulcerative Colitis in Japanese Individuals Using Population-specific SNP Array.


Journal

Inflammatory bowel diseases
ISSN: 1536-4844
Titre abrégé: Inflamm Bowel Dis
Pays: England
ID NLM: 9508162

Informations de publication

Date de publication:
17 07 2020
Historique:
received: 01 10 2019
pubmed: 20 2 2020
medline: 23 9 2021
entrez: 20 2 2020
Statut: ppublish

Résumé

To clarify the genetic background of ulcerative colitis (UC) in the Japanese population, we conducted a genome-wide association study (GWAS) using a population-specific single nucleotide polymorphism (SNP) array. We performed a GWAS and replication study including 1676 UC patients and 2381 healthy controls. The probability of colectomy was compared between genotypes of rs117506082, the top hit SNP at HLA loci, by the Kaplan-Meier method. We studied serum expression of miR-622, a newly identified candidate gene, from 32 UC patients and 8 healthy controls by quantitative reverse-transcription polymerase chain reaction. In the GWAS, only the HLA loci showed genome-wide significant associations with UC (rs117506082, P = 6.69E-28). Seven nominally significant regions included 2 known loci, IL23R (rs76418789, P = 6.29E-7) and IRF8 (rs16940202, P = 1.03E-6), and 5 novel loci: MIR622 (rs9560575, P = 8.23E-7), 14q31 (rs117618617, P = 1.53E-6), KAT6B (rs12260609, P = 1.81E-6), PAX3-CCDC140-SGPP2 (rs7589797, P = 2.87E-6), and KCNA2 (rs118020656, P = 4.01E-6). Combined analysis revealed that IL23R p.G149R (rs76418789, P = 9.03E-11; odds ratio [OR], 0.51) had genome-wide significant association with UC. Patients with GG genotype of rs117506082 had a significantly lower probability of total colectomy than those with the GA+AA genotype (P = 1.72E-2). Serum expression of miR-622 in patients with inactive UC tended to be higher than in healthy controls and patients with active UC (inactive UC vs healthy controls, P = 3.03E-02; inactive UC vs active UC, P = 6.44E-02). IL23R p.G149R is a susceptibility locus for UC in Japanese individuals. The GG genotype of rs117506082 at HLA loci may predict a better clinical course.

Sections du résumé

BACKGROUND
To clarify the genetic background of ulcerative colitis (UC) in the Japanese population, we conducted a genome-wide association study (GWAS) using a population-specific single nucleotide polymorphism (SNP) array.
METHODS
We performed a GWAS and replication study including 1676 UC patients and 2381 healthy controls. The probability of colectomy was compared between genotypes of rs117506082, the top hit SNP at HLA loci, by the Kaplan-Meier method. We studied serum expression of miR-622, a newly identified candidate gene, from 32 UC patients and 8 healthy controls by quantitative reverse-transcription polymerase chain reaction.
RESULTS
In the GWAS, only the HLA loci showed genome-wide significant associations with UC (rs117506082, P = 6.69E-28). Seven nominally significant regions included 2 known loci, IL23R (rs76418789, P = 6.29E-7) and IRF8 (rs16940202, P = 1.03E-6), and 5 novel loci: MIR622 (rs9560575, P = 8.23E-7), 14q31 (rs117618617, P = 1.53E-6), KAT6B (rs12260609, P = 1.81E-6), PAX3-CCDC140-SGPP2 (rs7589797, P = 2.87E-6), and KCNA2 (rs118020656, P = 4.01E-6). Combined analysis revealed that IL23R p.G149R (rs76418789, P = 9.03E-11; odds ratio [OR], 0.51) had genome-wide significant association with UC. Patients with GG genotype of rs117506082 had a significantly lower probability of total colectomy than those with the GA+AA genotype (P = 1.72E-2). Serum expression of miR-622 in patients with inactive UC tended to be higher than in healthy controls and patients with active UC (inactive UC vs healthy controls, P = 3.03E-02; inactive UC vs active UC, P = 6.44E-02).
CONCLUSIONS
IL23R p.G149R is a susceptibility locus for UC in Japanese individuals. The GG genotype of rs117506082 at HLA loci may predict a better clinical course.

Identifiants

pubmed: 32072174
pii: 5740361
doi: 10.1093/ibd/izaa033
doi:

Substances chimiques

HLA Antigens 0
IL23R protein, human 0
MIRN622 microRNA, human 0
MicroRNAs 0
Receptors, Interleukin 0

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1177-1187

Informations de copyright

© 2020 Crohn’s & Colitis Foundation. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Daisuke Okamoto (D)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yosuke Kawai (Y)

Genome Medical Science Project, National Center for Global Health and Medicine, Tokyo, Japan.

Yoichi Kakuta (Y)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Takeo Naito (T)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Takehiro Torisu (T)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Atsushi Hirano (A)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Junji Umeno (J)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Yuta Fuyuno (Y)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Dalin Li (D)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Takeru Nakano (T)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yasuhiro Izumiyama (Y)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Ryo Ichikawa (R)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Keiichiro Hiramoto (K)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Rintaro Moroi (R)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Masatake Kuroha (M)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yoshitake Kanazawa (Y)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Hisashi Shiga (H)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Katsushi Tokunaga (K)

Genome Medical Science Project, National Center for Global Health and Medicine, Tokyo, Japan.

Minoru Nakamura (M)

Clinical Research Center, National Hospital Organization (NHO), Nagasaki Medical Center, Omura, Japan.

Motohiro Esaki (M)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Division of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, Iwate Medical University, Morioka, Japan.

Takayuki Matsumoto (T)

F. Widjaja Family Foundation Inflammatory Bowel and Immunology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Health Administration Center, Center for the Advancement of Higher Education, Tohoku University, Sendai, Japan.

Dermot P B McGovern (DPB)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Masao Nagasaki (M)

Human Biosciences Unit for the Top Global Course Center for the Promotion of Interdisciplinary Education and Research (CPIER), Kyoto University, Kyoto, Japan.
Department of Endoscopic Diagnostics and Therapeutics, Saga University, Saga, Japan.

Yoshitaka Kinouchi (Y)

Department of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan.

Atsushi Masamune (A)

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.

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