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Methylation genes - U.S. Department of Veterans Affairs

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Last Updated: 15 February 2022

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DNA methylation protects against cisplatin-induced kidney injury by regulating specific genes, including interferon regulatory factor 8.

DNA methylation is an epigenetic device that regulates gene expression without altering primary nucleotide sequences. DNA methylation in mammals is based on the covalent addition of a methyl group to the 5-carbon position of cytosine by DNA methyltransferases. The evolution of DNA methylation and its pathological role in acute kidney injury remains largely unknown. In a rat kidney proximal tubular cell line, we first investigated the effects of DNA methylation inhibitor 5-aza-2'-deoxycytidine's antigenic tubular cell line to determine the pathological role of DNA methylation. We developed a kidney proximal tubule-specific DNMT1 knockout mouse model that had more AKI during cisplatin therapy than wild-type mice, which was consistent AKI during cisplatin therapy. The knockdown of Irf8 in the rat kidney tubular cells stifled cisplatin-induced apoptosis, leading to the discovery of the Irf8 gene in renal tubular cells, which supports a pro-death role of Irf8 in renal tubular cells.

Source link: https://doi.org/10.1016/j.kint.2017.03.038


Neonatal exposure to estradiol/bisphenol A alters promoter methylation and expression of Nsbp1 and Hpcal1 genes and transcriptional programs of Dnmt3a/b and Mbd2/4 in the rat prostate gland throughout life.

Evidence pointing to an early onset of prostate cancer is on the rise. We previously reported that neonatal rats' brief exposure to estradiol or bisphenol A elevated the risk of developing precancerous lesions in the prostate during androgen-supported therapy with estradiol as adults. Hypomethylation of the promoter of nucleosome binding protein-1, unlike Pde4d4, is an early and persistent epigenetic sign of neonatal exposure to estradiol/bisphenol A that persists throughout life, unaffected by adulthood events. Four of the eight genes involved in DNA methylation/demethylation showed early and persistent overexpression that was not a result of DNA methylation at their promoters, including genes encoding de novo DNA methyltransferases and demethylating domain proteins that have demethylating properties. We suspect that the distinctly different fate of early-life epigenetic marks during adulthood reflects the complex nature of lifelong epigenetic reprogramming's lifelong editing.

Source link: https://doi.org/10.1210/en.2011-1308

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions