ArticleMolecular genetics and genomics : MGG2015
A MCP-1 promoter polymorphism at G-2518A is associated with spontaneous preterm birth.
Article in Molecular genetics and genomics : MGG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Spontaneous preterm birth: advances toward the discovery of genetic predisposition.American journal of obstetrics and gynecology · 2018Review
- [Association between tumor necrosis factor-α G-308A polymorphisms and genetic susceptibility to spontaneous preterm birth].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- [Association between interleukin-1β C+3953T and genetic susceptibility to spontaneous preterm birth: a case-control study].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
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Authors and funding
5 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Monocyte chemoattractant protein-1 (MCP-1) is an important chemokine involved in the pathogenesis of spontaneous preterm birth (SPTB). We examined whether the MCP-1 G-2518A polymorphism is associated with the risk of SPTB in a Chinese population. The MCP-1 G-2518A polymorphism was genotyped in 569 preterm singleton neonates and in 673 term neonates using polymerase chain reaction-restriction fragment length polymorphism analysis. The distribution of the MCP-1 G-2518A genotype and the allele frequencies between the SPTB patients and the controls were not significantly different in the overall sample. However, we found that the AA genotype was associated with significantly increased susceptibility to very SPTB (<32 weeks) [odds ratio (OR) 2.07; 95 % confidence interval (CI), 1.27-3.36; P = 0.005) and extremely SPTB (<28 weeks) (OR 2.74; 95 % CI, 1.10-6.72; P = 0.014) compared with -2518G-positive genotypes (GG + GA genotypes). When extremely preterm neonates and very preterm neonates were combined, the AA genotype was also significantly associated with increased susceptibility to SPTB (OR 2.23; 95 % CI, 1.40-3.54; P < 0.001). The MCP-1 G-2518A polymorphism was not associated with increased susceptibility to SPTB in patients with premature rupture of the membranes (PROM) or in those without PROM. Our findings suggest that the MCP-1 G-2518A polymorphism may plays a role in mediating the susceptibility to SPTB in the Chinese population. Knowledge of genetic factors contributing to the pathogenesis of SPTB may have implications for screening and treatment of this disorder.
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