Cellular adaptation to environmental stress relies on a wide range of tightly controlled regulatory mechanisms, including transcription. Changes in chromatin structure and organization accompany the transcriptional response to stress, and in some cases, can impart memory of stress exposure to subsequent generations through mechanisms of epigenetic inheritance. In the budding yeast , histone post-translational modifications, and in particular histone methylation, have been shown to confer transcriptional memory of exposure to environmental stress conditions through mitotic divisions. Recent evidence from also implicates histone methylation in transgenerational inheritance of stress responses, suggesting a more widely conserved role in epigenetic memory.
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http://dx.doi.org/10.3390/cells8040339 | DOI Listing |
Cancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFNutrients
December 2024
Department of Translational Research, Western University of Health Sciences, Pomona, CA 91766, USA.
Background/objectives: Atherosclerosis is a chronic inflammatory disease developing and progressing in the presence of risk factors including hyperlipidemia, hypercholesterolemia, and chronic inflammation, among others. Atherosclerosis commonly precipitates as ischemic events, transient ischemic attacks, and myocardial infarction. Saturated fatty acids are risk factors; however, their association with epigenetics in the pathophysiology of atherosclerosis is not clearly understood.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Clinical Laboratory, School of Medicine, International University of Health and Welfare, Otawara 324-8501, Japan.
Intrauterine growth restriction (IUGR) is a risk factor for postnatal cardiovascular, metabolic, and psychiatric disorders. In most IUGR models, placental dysfunction that causes reduced 11β-hydroxysteroid dehydrogenase 2 (11βHSD2) activity, which degrades glucocorticoids (GCs) in the placenta, resulting in fetal GC overexposure. This overexposure to GCs continues to affect not only intrauterine fetal development itself, but also the metabolic status and neural activity in adulthood through epigenetic changes such as microRNA change, histone modification, and DNA methylation.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Gynecology and Obstetrics, University Medical Center Regensburg, 93935 Regensburg, Germany.
Cells
December 2024
School of Life Science, University of Technology Sydney, Ultimo, NSW 2007, Australia.
Chronic obstructive pulmonary disease (COPD) is characterized by progressive and incurable airflow obstruction and chronic inflammation. Both TGF-β1 and CXCL8 have been well described as fundamental to COPD progression. DNA methylation and histone acetylation, which are well-understood epigenetic mechanisms regulating gene expression, are associated with COPD progression.
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