ArticleBirth defects research. Part A, Clinical and molecular teratology2010
Gene expression profiling in the fetal cardiac tissue after folate and low-dose trichloroethylene exposure.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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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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.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Uncovering the Hidden Dangers and Molecular Mechanisms of Excess Folate: A Narrative Review.Nutrients · 2023Review
- Phagocytosing differentiated cell-fragments is a novel mechanism for controlling somatic stem cell differentiation within a short time frame.Cellular and molecular life sciences : CMLS · 2022Article
- Epigenetics and Congenital Heart Diseases.Journal of cardiovascular development and disease · 2022Review
- HNF4a transcription is a target of trichloroethylene toxicity in the embryonic mouse heart.Environmental science. Processes & impacts · 2020Article
- Trichloroethylene perturbs HNF4a expression and activity in the developing chick heart.Toxicology letters · 2018Article
- Biomarkers of Nutrition for Development-Folate Review.The Journal of nutrition · 2015Review
- Gene expression profiles in engineered cardiac tissues respond to mechanical loading and inhibition of tyrosine kinases.Physiological reports · 2013Article
- Human health effects of trichloroethylene: key findings and scientific issues.Environmental health perspectives · 2013Review
- Low-dose trichloroethylene alters cytochrome P450-2C subfamily expression in the developing chick heart.Cardiovascular toxicology · 2013Article
- Epigenetic alterations may regulate temporary reversal of CD4(+) T cell activation caused by trichloroethylene exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- The impact of folic acid supplementation on gestational and long term health: Critical temporal windows, benefits and risks.Porto biomedical journalReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrevious studies show gene expression alterations in rat embryo hearts and cell lines that correspond to the cardio-teratogenic effects of trichloroethylene (TCE) in animal models. One potential mechanism of TCE teratogenicity may be through altered regulation of calcium homeostatic genes with a corresponding inhibition of cardiac function. It has been suggested that TCE may interfere with the folic acid/methylation pathway in liver and kidney and alter gene regulation by epigenetic mechanisms. According to this hypothesis, folate supplementation in the maternal diet should counteract TCE effects on gene expression in the embryonic heart. APPROACH: To identify transcriptional targets altered in the embryonic heart after exposure to TCE, and possible protective effects of folate, we used DNA microarray technology to profile gene expression in embryonic mouse hearts with maternal TCE exposure and dietary changes in maternal folate.
resultsExposure to low doses of TCE (10 ppb) caused extensive alterations in transcripts encoding proteins involved in transport, ion channel, transcription, differentiation, cytoskeleton, cell cycle, and apoptosis. Exogenous folate did not offset the effects of TCE exposure on normal gene expression, and both high and low levels of folate produced additional significant changes in gene expression.
conclusionsA mechanism by which TCE induces a folate deficiency does not explain altered gene expression patterns in the embryonic mouse heart. The data further suggest that use of folate supplementation, in the presence of this toxin, may be detrimental and not protective of the developing embryo.
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