ArticlePloS one2016
Mono-(2-Ethylhexyl) Phthalate Promotes Pro-Labor Gene Expression in the Human Placenta.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Placental toxicity of alternative plasticizers: Current knowledge and future directions.Reproductive toxicology (Elmsford, N.Y.) · 2026Review
- Environmental Toxicants in the Hispanic Community Epigenetically Contributing to Preeclampsia.Cardiovascular toxicology · 2025Review
- Consumer Product Chemical Mixtures and Oxylipin-Mediated Inflammation and Oxidative Stress during Early Pregnancy: Findings from a Large US Pregnancy Cohort.Environmental science & technology · 2025Article
- Review
- Mono-(2-ethylhexyl) phthalate induces trophoblast hypoxia and mitochondrial dysfunction through HIF-1α-miR-210-3p axis in HTR-8/SVneo cell line.Current research in toxicology · 2024Article
- Review
- A study on the association of placental and maternal urinary phthalate metabolites.Journal of exposure science & environmental epidemiology · 2023Article
- Mono(2-ethylhexyl) phthalate induces transcriptomic changes in placental cells based on concentration, fetal sex, and trophoblast cell type.Archives of toxicology · 2023Article
- Role of microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health.Metabolites · 2022Review
- Cohort profile: the ECHO prenatal and early childhood pathways to health consortium (ECHO-PATHWAYS).BMJ open · 2022Article
- Expression of nuclear factor kappa B in ovine maternal inguinal lymph nodes during early pregnancy.BMC veterinary research · 2022Article
- Quercetin ameliorates Di (2-ethylhexyl) phthalate-induced nephrotoxicity by inhibiting NF-κB signaling pathway.Toxicology research · 2022Article
- Prenatal phthalate exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE cohort.Environment international · 2022Article
- Placental outcomes of phthalate exposure.Reproductive toxicology (Elmsford, N.Y.) · 2021Review
- Mechanistic insight into toxicity of phthalates, the involved receptors, and the role of Nrf2, NF-κB, and PI3K/AKT signaling pathways.Environmental science and pollution research international · 2021Review
- Association of biomarkers of exposure to metals and metalloids with maternal hormones in pregnant women from Puerto Rico.Environment international · 2021Article
- Placenta Disrupted: Endocrine Disrupting Chemicals and Pregnancy.Trends in endocrinology and metabolism: TEM · 2020Review
- Joint impact of phthalate exposure and stressful life events in pregnancy on preterm birth.Environment international · 2019Article
- Increased glucocorticoid receptor activity and proliferation in metastatic colon cancer.Scientific reports · 2019Article
- Associations of Phthalates and Phthalate Replacements With CRH and Other Hormones Among Pregnant Women in Puerto Rico.Journal of the Endocrine Society · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Women exposed to phthalates during pregnancy are at increased risk for delivering preterm, but the mechanism behind this relationship is unknown. Placental corticotropin-releasing hormone (CRH) and cyclooxygenase-2 (COX-2) are key mediators of parturition and are regulated by the non-canonical NF-kB (RelB/p52) signaling pathway. In this study, we demonstrate that one of the major phthalate metabolites, mono-(2-ethylhexyl)-phthalate (MEHP), increased CRH and COX-2 mRNA and protein abundance in a dose-dependent manner in primary cultures of cytotrophoblast. This was coupled with an increase in nuclear import of RelB/p52 and its association with the CRH and COX-2 promoters. Silencing of NF-kB inducing kinase, a central signaling component of the non-canonical NF-kB pathway, blocked MEHP-induced upregulation of CRH and COX-2. These results suggest a potential mechanism mediated by RelB/p52 by which phthalates could prematurely induce pro-labor gene activity and lead to preterm birth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.