ArticleJournal of molecular neuroscience : MN2015
DNA Methylation of the EphA5 Promoter Is Associated with Rat Congenital Hypothyroidism.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Brain development and bioenergetic changes.Neurobiology of disease · 2024Review
- CaMKIV mediates spine growth deficiency of hippocampal neurons by regulation of EGR3/BDNF signal axis in congenital hypothyroidism.Cell death discovery · 2022Article
- Identification of gene targets of developmental neurotoxicity focusing on DNA hypermethylation involved in irreversible disruption of hippocampal neurogenesis in rats.Journal of applied toxicology : JAT · 2021Article
- Congenital hypothyroidism impairs spine growth of dentate granule cells by downregulation of CaMKIV.Cell death discovery · 2021Article
- Genome-wide DNA methylation analysis of Hashimoto's thyroiditis during pregnancy.FEBS open bio · 2020Article
- c-Fos downregulation positively regulates EphA5 expression in a congenital hypothyroidism rat model.Journal of molecular histology · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormones (THs) are essential for normal development of the mammalian central nervous system through regulation of TH-responsive genes. EphA5, an important TH-responsive gene encoding the tyrosine kinase receptor EphA5, regulates synaptogenesis initiation and synaptic remodeling during brain development. Abnormal EphA5 expression is involved in the development of congenital hypothyroidism (CH). To show the regulatory mechanism of EphA5 expression in CH rats, we analyzed the correlation between methylation of the EphA5 promoter and its expression in the hypothyroid hippocampus and hippocampal neurons. Demethylation treatment using 5'-azadeoxycytidine upregulated EphA5 expression and rescued the effects of hypermethylation, suggesting a novel regulatory mechanism of EphA5 expression in CH rats. Our results suggest a potentially new approach for the development of drugs to restore neurocognitive impairments associated with CH.
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