ArticleEnvironmental health perspectives2005
Polychlorinated biphenyls disturb differentiation of normal human neural progenitor cells: clue for involvement of thyroid hormone receptors.
Article in Environmental health perspectives, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 150 citations in OpenAlex.
- Early-life exposure to PCBs and PFAS exerts negative effects on the developing central nervous system.Journal of hazardous materials · 2025Review
- Prenatal Exposure to Per- and Polyfluoroalkyl Substances, Maternal Thyroid Dysfunction, and Child Autism Spectrum Disorder.Endocrinology and metabolism (Seoul, Korea) · 2022Review
- Scientific Validation of Human Neurosphere Assays for Developmental Neurotoxicity Evaluation.Frontiers in toxicology · 2022Article
- Combining in vitro assays and mathematical modelling to study developmental neurotoxicity induced by chemical mixtures.Reproductive toxicology (Elmsford, N.Y.) · 2021Article
- Investigation of NH3 as a selective thyroid hormone receptor modulator in larval zebrafish (Danio rerio).Neurotoxicology · 2021Article
- Rabbit neurospheres as a novel in vitro tool for studying neurodevelopmental effects induced by intrauterine growth restriction.Stem cells translational medicine · 2021Article
- Exposure to prenatal PCBs shifts the timing of neurogenesis in the hypothalamus of developing rats.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2020Article
- Neurotoxicity of polychlorinated biphenyls and related organohalogens.Acta neuropathologica · 2019Review
- Comparative Analyses of the 12 Most Abundant PCB Congeners Detected in Human Maternal Serum for Activity at the Thyroid Hormone Receptor and Ryanodine Receptor.Environmental science & technology · 2019Article
- Strategies to improve the regulatory assessment of developmental neurotoxicity (DNT) using in vitro methods.Toxicology and applied pharmacology · 2018Article
- Article
- Disruption in Thyroid Signaling Pathway: A Mechanism for the Effect of Endocrine-Disrupting Chemicals on Child Neurodevelopment.Frontiers in endocrinology · 2018Review
- Combination of multiple neural crest migration assays to identify environmental toxicants from a proof-of-concept chemical library.Archives of toxicology · 2017Article
- Impairment of human neural crest cell migration by prolonged exposure to interferon-beta.Archives of toxicology · 2017Article
- Article
- A Preliminary Link between Hydroxylated Metabolites of Polychlorinated Biphenyls and Free Thyroxin in Humans.International journal of environmental research and public health · 2016Article
- Identification of transcriptome signatures and biomarkers specific for potential developmental toxicants inhibiting human neural crest cell migration.Archives of toxicology · 2016Article
- Measured Prenatal and Estimated Postnatal Levels of Polychlorinated Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children.Environmental health perspectives · 2015Article
- Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease.Endocrine-related cancer · 2014Review
- Developmental neurotoxicity - challenges in the 21st century and in vitro opportunities.ALTEX · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polychlorinated biphenyls (PCBs) are ubiquitous environmental chemicals that accumulate in adipose tissues over the food chain. Epidemiologic studies have indicated that PCBs influence brain development. Children who are exposed to PCBs during development suffer from neuropsychologic deficits such as a lower full-scale IQ (intelligence quotient), reduced visual recognition memory, and attention and motor deficits. The mechanisms leading to these effects are not fully understood. It has been speculated that PCBs may affect brain development by interfering with thyroid hormone (TH) signaling. Because most of the data are from animal studies, we established a model using primary normal human neural progenitor (NHNP) cells to determine if PCBs interfere with TH-dependent neural differentiation. NHNP cells differentiate into neurons, astrocytes, and oligodendrocytes in culture, and they express a variety of drug metabolism enzymes and nuclear receptors. Like triiodothyronine (T3), treatment with the mono-ortho-substituted PCB-118 (2,3',4,4 ,5-pentachlorobiphenyl; 0.01-1 microM) leads to a dose-dependent increase of oligodendrocyte formation. This effect was congener specific, because the coplanar PCB-126 (3,3',4,4 ,5-pentachlorobiphenyl) had no effect. Similar to the T3 response, the PCB-mediated effect on oligodendrocyte formation was blocked by retinoic acid and the thyroid hormone receptor antagonist NH-3. These results suggest that PCB-118 mimics T3 action via the TH pathway.
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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.