title: The SEPS1 G-105A polymorphism is associated with risk of spontaneous preterm birth in a Chinese population.
abstract: Inflammation plays an important role in the etiology and pathophysiology of spontaneous preterm birth (SPTB), and selenoprotein S (SEPS1) is involved in regulating the inflammatory response. Recently the G-105A promoter polymorphism in SEPS1 was shown to increase pro-inflammatory cytokine expression. We examined whether this functional polymorphism was related to the risk of SPTB in a Chinese population. We also examined the impact of premature rupture of membranes (PROM) on susceptibility to SPTB. The SEPS1 G-105A polymorphism was genotyped in 569 preterm singleton neonates and 673 term neonates by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. χ (2) tests and logistic regression analyses were used to calculate the odds ratios (ORs) and 95% confidence intervals (95% CIs). We observed that, compared with the GG genotype, -105A positive genotypes (GA + AA genotypes) were associated with significantly increased susceptibility to SPTB (adjusted OR, 1.87; 95% CI, 1.36-2.57; P<0.001). The -105A positive genotypes were also significantly associated with increased susceptibility to SPTB, both in the patients with PROM (adjusted OR, 2.65; 95% CI, 1.73-4.03; P<0.001) and in those without PROM (adjusted OR, 1.56; 95% CI, 1.09-2.24; P = 0.015). The -105A positive genotypes were also significantly associated with increased susceptibility to SPTB between extremely preterm neonates and controls (adjusted OR, 4.46; 95% CI, 1.86-10.73; P = 0.002) and between moderately preterm neonates and controls (adjusted OR, 1.76; 95% CI, 1.25-2.47; P = 0.001). Our findings suggest that the SEPS1 G-105A polymorphism contributes to the risk of developing SPTB in a Chinese population.
authors.affiliation: BaYi Children's Hospital, General Military Hospital of Beijing PLA, PR China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Xiao
authors.initials: X
authors.lastname: Yang
authors.forename: Yong
authors.initials: Y
authors.lastname: Zheng
authors.forename: Zhi-Hao
authors.initials: ZH
authors.lastname: Wu
authors.forename: Xiao-Ai
authors.initials: XA
authors.lastname: Zhang
authors.forename: Qiu-Ping
authors.initials: QP
authors.lastname: Li
authors.forename: Xi-Yu
authors.initials: XY
authors.lastname: He
authors.forename: Chun-Zhi
authors.initials: CZ
authors.lastname: Wang
authors.forename: Zhi-Chun
authors.initials: ZC
authors.lastname: Feng
mesh_terms: D000328:Adult; D000483:Alleles; D044466:Asian People; D005260:Female; D005838:Genotype; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length / Q000235:genetics; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011247:Pregnancy; D047928:Premature Birth / Q000235:genetics*; D051140:Selenoproteins / Q000235:genetics*
chemical_list: D008565:Membrane Proteins; C487710:SELENOS protein, human; D051140:Selenoproteins