ArticleReproductive biology and endocrinology : RB&E2015
Mono-ethylhexyl phthalate stimulates prostaglandin secretion in human placental macrophages and THP-1 cells.
Article in Reproductive biology and endocrinology : RB&E, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Placental toxicity of alternative plasticizers: Current knowledge and future directions.Reproductive toxicology (Elmsford, N.Y.) · 2026Review
- Evaluating impacts of the trichloroethylene metaboliteJournal of immunotoxicology · 2025Article
- Impact of endocrine disrupting chemicals on macrophages at the maternal-fetal interface.Seminars in immunopathology · 2025Review
- Palmitate and group BFrontiers in immunology · 2024Article
- The Impact of Chronic Phthalate Exposure on Rodent Anxiety and Cognition.Biological psychiatry global open science · 2024Review
- Associations of phthalates, phthalate replacements, and their mixtures with eicosanoid biomarkers during pregnancy.Environment international · 2023Article
- Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy.Molecular systems biology · 2023Article
- 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
- Impact of mono(2-ethylhexyl) phthalate (MEHP) on the development of mouse embryo in vitro.Reproductive toxicology (Elmsford, N.Y.) · 2023Article
- Streptococcus agalactiaemBio · 2022Article
- The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine inhibits lipopolysaccharide-induced inflammation transcriptomic pathways and cytokine secretion in a macrophage cell model.Toxicology in vitro : an international journal published in association with BIBRA · 2022Article
- Streptococcus agalactiae cadD alleviates metal stress and promotes intracellular survival in macrophages and ascending infection during pregnancy.Nature communications · 2022Article
- Placental outcomes of phthalate exposure.Reproductive toxicology (Elmsford, N.Y.) · 2021Review
- Endocrine Disruptor Compounds-A Cause of Impaired Immune Tolerance Driving Inflammatory Disorders of Pregnancy?Frontiers in endocrinology · 2021Review
- Exposure to Phenols, Phthalates, and Parabens and Development of Metabolic Syndrome Among Mexican Women in Midlife.Frontiers in public health · 2021Article
- Placenta Disrupted: Endocrine Disrupting Chemicals and Pregnancy.Trends in endocrinology and metabolism: TEM · 2020Review
- Palmitate induces apoptotic cell death and inflammasome activation in human placental macrophages.Placenta · 2020Article
- Macrophage Plasticity in Reproduction and Environmental Influences on Their Function.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDiethylhexyl phthalate (DEHP) is widely used as a plasticizer in polyvinyl chloride products. DEHP exposure, which is widespread in the US, increases preterm birth risk; however, the mechanisms driving this relationship are unclear. Because cyclooxygenase-2 (COX-2) dependent prostaglandin synthesis is implicated in preterm birth, we evaluated effects of mono-2-ethylhexyl phthalate (MEHP), the active metabolite of DEHP, on prostaglandin E2 (PGE2) synthesis and COX expression in human placental macrophages (PM). In addition, responses in PM were compared to those in a human macrophage-like cell line, THP-1.
methodsPM and THP-1 cells were treated for 2, 4, 8, or 24 h with MEHP concentrations ranging from 10 to 180 micromolar. PGE2 concentrations were assessed in culture medium using ELISA, and COX expression was determined by western blot.
resultsTreatment of PM and THP-1 cells with 180 micromolar MEHP for 24 h significantly increased PGE2 release. Co-treatment of PMs or THP-1 cells with 180 micromolar MEHP and the non-selective COX inhibitor indomethacin reduced MEHP-stimulated PGE2 production. Similarly, co-treatment of PM and THP-1 cells with the COX-2 selective inhibitor NS-398 resulted in a significant decrease in PGE2, suggesting that MEHP-stimulated PGE2 is dependent specifically on increased COX-2 expression. Western blot analysis revealed a significant increase in COX-2 expression in PM and THP-1 cells treated with 180 micromolar MEHP, and no changes in COX-1 expression, supporting the role of COX-2 in MEHP-stimulated PGE2 synthesis.
conclusionsThe findings from this study are the first to demonstrate phthalate-stimulated PGE2 synthesis in PM and warrant future studies into COX-2-dependent prostaglandin synthesis as a mechanism of toxicant-associated 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.