ArticleNeurotoxicology and teratology
Reduced expression of MAPK/ERK genes in perinatal arsenic-exposed offspring induced by glucocorticoid receptor deficits.
Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway.Molecular medicine reports · 2018Pooled it
- Sirtuins as mediators and targets of arsenic toxicity: unraveling signaling pathway crosstalk.Archives of toxicology · 2025Review
- Mechanisms Associated with Cognitive and Behavioral Impairment Induced by Arsenic Exposure.Cells · 2023Review
- Developmental Exposure to Endocrine Disrupting Chemicals and Its Impact on Cardio-Metabolic-Renal Health.Frontiers in toxicology · 2021Review
- Is prenatal arsenic exposure associated with salivary cortisol in infants in Arica, Chile? An exploratory cohort study.Annals of agricultural and environmental medicine : AAEM · 2019Article
- Review
- Molecular insight of arsenic-induced carcinogenesis and its prevention.Naunyn-Schmiedeberg's archives of pharmacology · 2017Review
- Oncogenomic disruptions in arsenic-induced carcinogenesis.Oncotarget · 2017Review
- Developmental exposure to 50 parts-per-billion arsenic influences histone modifications and associated epigenetic machinery in a region- and sex-specific manner in the adult mouse brain.Toxicology and applied pharmacology · 2015Article
- Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain.Toxicology reports · 2015Article
- Surgical stress induces brain-derived neurotrophic factor reduction and postoperative cognitive dysfunction via glucocorticoid receptor phosphorylation in aged mice.CNS neuroscience & therapeutics · 2015Article
- Inhibition of phosphodiesterase 2 reverses impaired cognition and neuronal remodeling caused by chronic stress.Neurobiology of aging · 2015Article
- Fluoxetine treatment ameliorates depression induced by perinatal arsenic exposure via a neurogenic mechanism.Neurotoxicology · 2014Article
- Ethanol induced acetylation of histone at G9a exon1 and G9a-mediated histone H3 dimethylation leads to neurodegeneration in neonatal mice.Neuroscience · 2014Article
- The Effects of Arsenic Exposure on Neurological and Cognitive Dysfunction in Human and Rodent Studies: A Review.Current environmental health reports · 2014Review
- Article
- Perinatal exposure to 50 ppb sodium arsenate induces hypothalamic-pituitary-adrenal axis dysregulation in male C57BL/6 mice.Neurotoxicology · 2012Article
- The epigenetic lorax: gene-environment interactions in human health.Epigenomics · 2012Review
- Prenatal arsenic exposure alters the programming of the glucocorticoid signaling system during embryonic development.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Changes within the glucocorticoid receptor (GR) cellular signaling pathway were evaluated in adolescent mice exposed to 50 ppb arsenic during gestation. Previously, we reported increased basal plasma corticosterone levels, decreased hippocampal GR levels and deficits in learning and memory performance in perinatal arsenic-exposed mice. The biosynthesis of members of the mitogen-activated protein kinase (MAPK) signaling pathway, known to be involved in learning and memory, is modulated by the binding of GR to glucocorticoid response elements (GREs) in the gene promoters. Two genes of the MAPK pathway, Ras and Raf, contain GREs which are activated upon binding of GRs. We evaluated the activity of GRs at Ras and Raf promoters using chromatin immunoprecipitation and real-time PCR and report decreased binding of the GR at these promoters. An ELISA-based GR binding assay was used to explore whether this decreased binding was restricted to in vivo promoters and revealed no differences in binding of native GR to synthetic GREs. The decreased in vivo GR binding coincides with significantly decreased mRNA levels and slight reductions of protein of both H-Ras and Raf-1 in perinatally arsenic-exposed mice. Nuclear activated extracellular-signal regulated kinase (ERK), a downstream target of Ras and Raf, whose transcriptional targets also play an important role in learning and memory, was decreased in the hippocampus of arsenic-exposed animals when compared to controls. GR-mediated transcriptional deficits in the MAPK/ERK pathway could be an underlying cause of previously reported learning deficits and provide the link to arsenic-induced deficiencies in cognitive development.
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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.