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Placental genetic variations in circadian clock-related genes increase the risk of placental abruption

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Authors
Chunfang, Qiu
Gelaye, Bizu
Denis, Marie
Tadesse, Mahlet G.
Enquobahrie, Daniel A.
Ananth, Cande V.
Pacora, Percy N.
Salazar, Manuel
Sanchez, Sixto E.
Williams, Michelle A.
Issue Date
2016-03
Keywords
Circadian gene
Placental abruption
Pregnancy
Pregnancy
Placentae
SNPs
xmlui.metadata.dc.contributor.email
Chun-fang.Qiu@Swedish.org

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Publisher
International Journal of Molecular Epidemiology and Genetics
Journal
International Journal of Molecular Epidemiology and Genetics (Int J Mol Epidemiol Genet)
URI
http://hdl.handle.net/10757/607302
Additional Links
http://www.ijmeg.org/IJMEG_V7N1.html
Abstract
The genetic architecture of placental abruption (PA) remains poorly understood. We examined variations in SNPs of circadian clock-related genes in placenta with PA risk. We also explored placental and maternal genomic contributions to PA risk. Placental genomic DNA samples were isolated from 280 PA cases and 244 controls. Genotyping was performed using the Illumina Cardio-MetaboChip. We examined 116 SNPs in 13 genes known to moderate circadian rhythms. Logistic regression models were fit to estimate odds ratios (ORs). The combined effect of multiple SNPs on PA risk was estimated using a weighted genetic risk score. We examined independent and joint associations of wGRS derived from placental and maternal genomes with PA. Seven SNPs in five genes (ARNTL2, CRY2, DEC1, PER3 and RORA), in the placental genome, were associated with PA risk. Each copy of the minor allele (G) of a SNP in the RORA gene (rs2899663) was associated with a 30% reduced odds of PA (95% CI 0.52-0.95). The odds of PA increased with increasing placental-wGRS (Ptrend<0.001). The ORs were 1.00, 2.16, 3.24 and 4.48 across quartiles. Associations persisted after the maternal-wGRS was included in the model. There was evidence of an additive contribution of placental and maternal genetic contributions to PA risk. Participants with placental- and maternal-wGRS in the highest quartile, compared with those in the lowest quartile, had a 15.57-fold (95% CI 3.34- 72.60) increased odds of PA. Placental variants in circadian clock-related genes are associated with PA risk; and the association persists after control of genetic variants in the maternal genome
Type
info:eu-repo/semantics/article
Rights
info:eu-repo/semantics/openAccess
Language
eng
ISSN
1948-1756
Collections
Medicina

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