Fetal alcohol spectrum disorder (FASD) affects the hippocampal levels of histone variant H2A.Z-2
العنوان: | Fetal alcohol spectrum disorder (FASD) affects the hippocampal levels of histone variant H2A.Z-2 |
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المؤلفون: | María González-Perez, Monica Tyagi, Melissa E. Freeman, Manjinder S. Cheema, Taylor L. Gretzinger, Brian R. Christie, Christine J. Fontaine, Juan Ausió |
المصدر: | Biochemistry and Cell Biology. 97:431-436 |
بيانات النشر: | Canadian Science Publishing, 2019. |
سنة النشر: | 2019 |
مصطلحات موضوعية: | medicine.medical_specialty, Methyl-CpG-Binding Protein 2, Alcohol, Hippocampal formation, Hippocampus, Biochemistry, MECP2, Histones, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, Animals, Medicine, Epigenetics, Molecular Biology, 030304 developmental biology, 0303 health sciences, Ethanol, biology, business.industry, Gene Expression Profiling, Cell Biology, Rats, Chromatin, Histone, Endocrinology, chemistry, Fetal Alcohol Spectrum Disorders, Fetal Alcohol Spectrum Disorder, biology.protein, Female, business, 030217 neurology & neurosurgery |
الوصف: | Fetal alcohol spectrum disorder (FASD) is caused by prenatal exposure to ethanol and has been linked to neurodevelopmental impairments. Alcohol has the potential to alter some of the epigenetic components that play a critical role during development. Previous studies have provided evidence that prenatal exposure to ethanol results in abnormal epigenetic patterns (i.e., hypomethylation) of the genome. The aim of this study was to determine how prenatal exposure to ethanol in rats affects the hippocampal levels of expression of two important brain epigenetic transcriptional regulators involved in synaptic plasticity and memory consolidation: methyl CpG-binding protein 2 (MeCP2) and histone variant H2A.Z. Unexpectedly, under the conditions used in this work we were not able to detect any changes in MeCP2. Interestingly, however, we observed a significant decrease in H2A.Z, accompanied by its chromatin redistribution in both female and male FASD rat pups. Moreover, the data from reverse-transcription qPCR later confirmed that this decrease in H2A.Z is mainly due to down-regulation of its H2A.Z-2 isoform gene expression. Altogether, these data provide strong evidence that prenatal exposure to ethanol alters histone variant H2A.Z during neurogenesis of rat hippocampus. |
تدمد: | 1208-6002 0829-8211 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d47c9810528f518466fd06300a901d67 https://doi.org/10.1139/bcb-2018-0240 |
حقوق: | CLOSED |
رقم الأكسشن: | edsair.doi.dedup.....d47c9810528f518466fd06300a901d67 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 12086002 08298211 |
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