Integrative analysis highlighted susceptibility genes for rheumatoid arthritis.

Autor: Mo XB; Center for Genetic Epidemiology and Genomics, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Department of Epidemiology, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China., Sun YH; Center for Genetic Epidemiology and Genomics, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Department of Epidemiology, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China., Zhang YH; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Department of Epidemiology, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China., Lei SF; Center for Genetic Epidemiology and Genomics, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China; Department of Epidemiology, School of Public Health, Medical College of Soochow University, 199 Renai Road, Suzhou, Jiangsu 215123, PR China. Electronic address: leisf@suda.edu.cn.
Jazyk: angličtina
Zdroj: International immunopharmacology [Int Immunopharmacol] 2020 Sep; Vol. 86, pp. 106716. Date of Electronic Publication: 2020 Jun 26.
DOI: 10.1016/j.intimp.2020.106716
Abstrakt: Genetic factors underlying susceptibility to rheumatoid arthritis (RA) are largely unknown. The aim of this study was to identify potential genes for RA. We conducted summary statistic data-based Mendelian randomization (SMR) analysis to detect potential causal genes for RA. Further, we performed additional bioinformatics analysis to show the potential relevance of the identified genes to RA. We identified 140 genes that showed causal association with RA. Among these genes, 24 have not been reported to be associated with RA (e.g., IFNAR2, FLOT1, ITPR3, PPP2R3C and SLC35B2). The unreported genes were highly connected with some well-known RA-related genes (e.g., HLA-DQB1, CD226, PTPN22, CD40, IFNGR2, BLK, TRAF1, SYNGR1 and CCR6) that were also found to be causally associated with RA. The identified genes were involved in the significant enriched RA-related biological pathways. We found integrative evidence in support of IFNAR2 as a potential causal gene of RA in SMR, differential expression, weighted gene co-expression network, protein-protein interaction and functional enrichment analyses. The present study highlights a list of potential causal genes for RA. The findings provide new insights into the mechanism underlying known genome-wide associated RA susceptibility loci.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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