Association of a functional polymorphism in the 3′-untranslated region of SPI1 with systemic lupus erythematosus
Abstract
OBJECTIVE: SPI1, also referred to as PU.1, is an Ets family transcription factor that interacts with IRF2, IRF4, and IRF8. In view of the significance of the type I interferon pathway in systemic lupus erythematosus (SLE), this study was undertaken to investigate a possible association between SPI1 polymorphisms and SLE. METHODS: A case-control association study was performed using 6 tag single-nucleotide polymorphisms (SNPs), as well as a SNP located upstream of SPI1 previously found to be associated with acute myelogenous leukemia, in 400 Japanese patients with SLE and 450 healthy controls. Resequencing of all exons and known regulatory regions was performed to identify functional polymorphisms. Association of genotype and SPI1 expression was examined using the GENEVAR database and reporter assays. RESULTS: A significant association was detected in 2 SNPs in intron 2 (rs10769258 and rs4752829) (P = 0.005 and P = 0.008, respectively, under the dominant model). The association was stronger in patients with nephropathy. Resequencing identified a potentially functional polymorphism in the 3'-untranslated region (3'-UTR), rs1057233, which was in strong linkage disequilibrium with the SNPs in intron 2. The number of risk alleles at rs1057233 was strongly correlated with SPI1 messenger RNA (mRNA) level in the database analysis (P = 0.0002), and was confirmed by a reporter assay. Interestingly, rs1057233 alters a target sequence for microRNA hsa-miR-569 (miR-569). Transfection experiments demonstrated that miR-569 inhibits expression of a reporter construct with the 3'-UTR sequence containing the nonrisk allele but not the risk allele. CONCLUSION: Our findings indicate that a SNP in the 3'-UTR of SPI1 is associated with elevated SPI1 mRNA level and with susceptibility to SLE.
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Colocalization analyses using coloc and SMR/HEIDI support the hypothesis that the same causal SNP(s) influence SPI1 expression and AD risk.
“Colocalization analyses using coloc32 and SMR/HEIDI23 support the hypothesis that the same causal SNP(s) influence SPI1 expression and AD risk.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [32]
rs1057233 resides in the 3'-UTR of SPI1.
“Moreover, rs1057233 resides in the 3’-UTR of SPI1, which is a target binding site of miRNAs [43].”
From Association of SPI1 haplotypes with altered SPI1 gene expression and Alzheimer’s disease risk (2022) · cites this paper as [43]
The 3'-UTR of SPI1 is a target binding site of miRNAs.
“Moreover, rs1057233 resides in the 3’-UTR of SPI1, which is a target binding site of miRNAs [43].”
From Association of SPI1 haplotypes with altered SPI1 gene expression and Alzheimer’s disease risk (2022) · cites this paper as [43]
hsa-miR-569 binding with the 3'-UTR of SPI1 is affected by rs1057233.
“we identified hsa-miR–569, whose binding with the 3’-UTR of SPI1 is reportedly affected by rs1057233 [43]”
From Association of SPI1 haplotypes with altered SPI1 gene expression and Alzheimer’s disease risk (2022) · cites this paper as [43]
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- Authors
- Hikami, K., Kawasaki, A., Ito, I., Koga, M., Ito, S., Hayashi, T., Matsumoto, I., Tsutsumi, A., Kusaoi, M., Takasaki, Y., Hashimoto, H., Arinami, T., Sumida, T., & Tsuchiya, N.
- Affiliations
- University of Tsukuba (JP)
- Juntendo University (JP)
- ORCID
- Venue
- Arthritis & Rheumatism
- Publisher
- Wiley
- Published
- 2011-02-25
- Volume
- 63
- Issue
- 3
- Pages
- 755-763
- ISSN
- 0004-3591 (ISSN-L)
- OpenAlex
- W2042023916
- Cited by
- 58
- References
- 48
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 1 · 2023: 1 · 2022: 9 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 7 · 2014: 8 · 2013: 5 · 2012: 5
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arthritis & Rheumatism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (21591260, 22390199)
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Keywords
- systemic lupus erythematosus, PU.1, 3' untranslated region, single nucleotide polymorphisms, genetic susceptibility, miRNA target genes, mRNA expression, kidney disease, type I interferon pathway, ETS transcription factors, Japanese patients
- MeSH terms
- Proto-Oncogene Protein Spi-1, Adult, Female, Genotype, Humans, Lupus Erythematosus, Systemic, Male, Middle Aged, Proto-Oncogene Proteins, Risk Factors, Transfection, Trans-Activators, Linkage Disequilibrium, Genes, Reporter, Genetic Predisposition to Disease, 3' Untranslated Regions, Polymorphism, Single Nucleotide, MicroRNAs, Asian People, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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