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Title: Epigenetic Regulation of the Nitric Oxide Pathway, 17-α Hydroxyprogesterone Caproate, and Recurrent Preterm Birth.

Authors: Manuck, Tracy A; Smeester, Lisa; Martin, Elizabeth M; Tomlinson, Martha S; Smith, Christina; Varner, Michael W; Fry, Rebecca C

Published In Am J Perinatol, (2018 07)

Abstract: We sought to evaluate nitric oxide pathway placental gene expression and the epigenome (CpG methylation) among women receiving 17-α hydroxyprogesterone caproate (17-OHPC) with and without recurrent preterm birth (PTB).This was a case-control study. We prospectively recruited women with ≥ 1 prior singleton spontaneous PTB <34 weeks receiving 17-OHPC. DNA and RNA were isolated from placentas. RNA abundance (gene expression) and the methylome were analyzed for 84 genes in nitric oxide pathways. Women with recurrent PTB <34 weeks (cases) were compared with those delivering at term (controls). Statistical analysis included multivariable models with Bonferroni's corrected p-values.In this study, 17 women met inclusion criteria; 7 preterm cases (delivered at 22.6 ± 2.9 weeks) and 10 term controls (delivered at 38.5 ± 0.8 weeks). Groups had similar PTB history, race/ethnicity, and socioeconomic risk factors for PTB. Twenty-seven nitric oxide genes displayed differential expression (p < 0.05 and q < 0.10) when comparing placentas from preterm cases and term controls; all were downregulated in preterm cases. Eight hundred sixty corresponding CpG sites were differentially methylated between the preterm cases and term controls (Bonferroni's p-value <0.05).CpG methylation and gene expression patterns in nitric oxide pathway genes differ among placentas from recurrent PTB compared with term birth following 17-OHPC exposure.

PubMed ID: 29241278 Exiting the NIEHS site

MeSH Terms: 17 alpha-Hydroxyprogesterone Caproate/therapeutic use*; Adult; Case-Control Studies; CpG Islands; Epigenesis, Genetic; Estrogen Antagonists/therapeutic use*; Female; Gene Expression; Gestational Age; Humans; Infant, Newborn; Methylation; Nitric Oxide/metabolism*; Pregnancy; Premature Birth/genetics*; Premature Birth/prevention & control*; Prospective Studies; Recurrence; Risk Factors; Signal Transduction*

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