ArticleEnvironmental health perspectives2011
Retinoic acid drives aryl hydrocarbon receptor expression and is instrumental to dioxin-induced toxicity during palate development.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 39 citations in OpenAlex.
- Craniofacial and dental toxicity of dioxins: developmental phenotypes and mechanistic insights.Frontiers in cell and developmental biology · 2026Review
- Developmental exposure to 1,4-dioxane, a volatile organic compound of emerging concern, induces immediate phenotypic, transcriptomic, and adult-onset neurodevelopmental effects.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Exposure to the persistent organic pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) disrupts development of the zebrafish inner ear.Aquatic toxicology (Amsterdam, Netherlands) · 2023Article
- Retinoic acid effects on in vitro palatal fusion and WNT signaling.European journal of oral sciences · 2022Article
- Mathematical modeling of palatal suture pattern formation: morphological differences between sagittal and palatal sutures.Scientific reports · 2021Article
- Gene-Environment Interplay and MicroRNAs in Cleft Lip and Cleft Palate.Oral science international · 2021Article
- Environmental mechanisms of orofacial clefts.Birth defects research · 2020Review
- Meta-Analysis of Transcriptome Data Detected New Potential Players in Response to Dioxin Exposure in Humans.International journal of molecular sciences · 2020Article
- Copy Number Changes Identified Using Whole Exome Sequencing in Nonsyndromic Cleft Lip and Palate in a Honduran Population.Birth defects research · 2017Article
- TCF21 and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells.PLoS genetics · 2017Article
- Long non-coding RNA H19-mediated mouse cleft palate induced by 2,3,7,8-tetrachlorodibenzo-Experimental and therapeutic medicine · 2016Article
- AHR Function in Lymphocytes: Emerging Concepts.Trends in immunology · 2016Review
- Gene-Environment Interactions Target Mitogen-activated Protein 3 Kinase 1 (MAP3K1) Signaling in Eyelid Morphogenesis.The Journal of biological chemistry · 2015Article
- Retinoid-xenobiotic interactions: the Ying and the Yang.Hepatobiliary surgery and nutrition · 2015Review
- Triphenyl phosphate-induced developmental toxicity in zebrafish: potential role of the retinoic acid receptor.Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- Craniofacial form is altered by chronic adult exposure to 2,3,7,8-tetrachlorodibenzo-Toxicology reports · 2015Article
- Windows of Sensitivity to Toxic Chemicals in the Development of Cleft Palates.Journal of toxicology and environmental health. Part B, Critical reviews · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPalate development depends on complex events and is very sensitive to disruption. Accordingly, clefts are the most common congenital malformations worldwide, and a connection is proposed with fetal exposure to toxic factors or environmental contaminants, such as dioxins. There is increasing evidence that dioxin interferes with all-trans-retinoic acid (atRA), a hormone-like signal derived from vitamin A, which plays an essential role during embryonic development. Although similarities have been described between dioxin-induced toxicity and the outcome of altered atRA signaling during palate development, their relationship needs to be clarified.
objectivesWe used a genetic approach to understand the interaction between atRA and dioxin and to identify the cell type targeted by dioxin toxicity during secondary palate formation in mice.
methodsWe analyzed the phenotype of mouse embryos harboring an atRA-sensitive reporter transgene or bearing null mutations for atRA-synthesizing enzymes (RALDH) or atRA receptors (RAR) and maternally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at gestation day 10.5.
resultsWe found that an intact atRA signal was required to enable TCDD to induce cleft palate. This mandatory atRA signal was generated through the activity of RALDH3 in the nasal epithelium and was transduced by RARγ (RARG) in the nasal mesenchyme, where it notably controlled aryl hydrocarbon receptor (Ahr) transcript levels. TCDD also did not alter the developmental pattern of atRA signaling during palate formation.
conclusionsTCDD-induced alteration of secondary palate development in the mouse appears to depend on atRA signaling, which controls AHR expression. This mechanism is likely conserved throughout vertebrate evolution and may therefore be relevant in humans.
Indexed as
Identifiers
What OpenQuestion holds
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.