A miRNA-492 binding-site polymorphism in BSG (basigin) confers risk to psoriasis in Central South Chinese population View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-06-08

AUTHORS

Li-Sha Wu, Fang-Fang Li, Liang-Dan Sun, Dai Li, Juan Su, Ye-Hong Kuang, Gang Chen, Xiao-Ping Chen, Xiang Chen

ABSTRACT

Psoriasis (PS; MIM#177900) is a chronic inflammatory immune-mediated skin disorder. Although the disease is believed to be caused by a combination of genetic, immunologic and environmental factors, its complete etiology has not been fully understood. Here, we focused on the BSG (MIM#109480), a member of the immunoglobulin superfamily expressed ubiquitously in circulating immune cell populations. We observed that the expression level of BSG in PBMCs was elevated in psoriasis patients. To understand the underlying mechanism for this change, we genotyped the rs8259 T>A SNP located in the 3′UTR of the BSG gene from 668 psoriasis patients and 1,143 healthy controls. The rs8259 T allele was associated with significantly decreased psoriasis susceptibility (OR = 0.758, 95% CI 0.638–0.901, p = 0.002). Interestingly, the rs8259 polymorphism was located in a seed region for miR-492 binding. The miR-492 was able to bind to the BSG 3′UTR sequence bearing the rs8259 T allele as assayed by luciferase reporter gene assay. The substitution of T with A abolished miR-492 binding. BSG protein expression in PBMCs from patients carrying the rs8259 AA genotype was significantly higher than in those from patients carrying the rs8259 TT genotype. Our study suggests that miR-492 may physiologically suppress BSG expression and the BSG rs8259 polymorphism is associated with decreased psoriasis susceptibility through affecting miR-492 binding. More... »

PAGES

749-757

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00439-011-1026-5

DOI

http://dx.doi.org/10.1007/s00439-011-1026-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009241823

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21655935


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