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This paper examines recent advances in the use of psychostimulant use on redox-imbalance-induced DNA methylation to create novel epigenetics-based early interventions. Results: Intestability in DNA methylation signatures and redox expression in various research models stimulated by psychostimulants and opioids has been demonstrated in several research studies, illustrating the widespread presence of epigenetic shifts in DNA methylation signatures in neurological disorders. This review summarizes the need for more research and experimental studies of DNA-methylation-based therapies that may help to determine whether psychostimulant use and oxidative stress or redox-linked metabolic recalibration impact neuronal impairments.
Source link: https://europepmc.org/article/MED/35227168
Heterochromatin is the most compacted form of chromatin with various condensation characteristics characterized by high DNA methylation. Here, we investigate the mechanism of MeCP2-driven heterochromatin coordination and dynamics by combining liquid-liquid phase separation and single-molecule analysis with quantification of local MeCP2 concentrations in vitro and in vivo. MeCP2 LLPS and slower MeCP2 mobility are promoted by Crowded environments and DNA, which also supports MeCP2 LLPS and slower MeCP2 mobility. In the minimal in vitro model, we are able to model the heterochromatin compartmentalization, as well as MeCP2 concentration and heterogeneous motion.
Source link: https://europepmc.org/article/MED/35156529
Both head and neck squamous cell carcinomas, as well as head and neck squamous cell carcinomas, are under scrutiny by the tumor necrosis factor receptor superfamily members 4 and 18 as potential targets for immunotherapy of various cancers, including head and neck squamous cell carcinomas. The Cancer Genome Atlas Research Network conducted broad comparative analysis of DNA methylation of 46 CpG sites within the GITR/OX40 gene locus in head and neck squamous cell carcinomas and normal adjacent tissues. In addition, we investigated methylation levels in HPV-positive and HPV-negative cell lines and in isolated monocytes, granulocytes, CD8+ and CD4+ T cells from healthy donors' peripheral blood. We found significant methylation differences between normal adjacent and tumor tissues, between HPV-positive and HPV-negative tumors, between tumor and immune cells, as well as strong correlations between methylation and mRNA expression, as well as strong correlations between tumor and immune cells. CpG methylation correlations were also found with overall survival, signs of immune cell infiltrate infiltrates, an interferon-based signature, and mutational load.
Source link: https://europepmc.org/article/MED/34908008
Phenolic acids form a large variety of phytochemical molecules present in the plant kingdom; they play a vital role as epigenetic regulators, particularly as inhibitors of DNA methylation. They were then tested for their cytotoxic effects on hepatic carcinoma cells and immortalized human hepatocyte cells. In addition, its effect on Hep3B's global DNA methylation inhibition was also established. The cinnamic derivatives 11-14 and 20-22 were more potent than free caffeic acid, being methyl 3,4-dihydroxycinammate the most active with an IC 50 = 109. 7 0. 8 M.
Source link: https://europepmc.org/article/MED/35451561
Lung epithelium-specific DNA methylation patterns can possibly reveal the presence of lung-derived cell-free DNA in blood, providing an indication of lung cell death. People with advanced lung cancer have a significant rise in lung cfDNA levels in blood. In the plasma of those who have bronchoscopy or other lung disease patients, lung-derived cfDNA is found in those who have lung cancer and to a lesser extent in those diagnosed with other respiratory diseases. In patients with acute exacerbation of chronic pulmonary disease with intermittent inflammation compared to patients with stable disease, Lung cfDNA is also elevated in patients with acute exacerbation of chronic obstructive pulmonary disease, which is also associated with future exacerbation and mortality in these patients. Conclusions Universal cfDNA methylation markers of normal lung epithelium allow for mutation-independent, fast, and specific detection of lung-derived cfDNA, which is a topic of ongoing lung disease research.
Source link: https://europepmc.org/article/MED/35450968
We obtained DNA methylation results from n = 100 opossum samples from the ear, liver, and tail using the mammalian methylation array. We compared postnatal growth and later aging in the opossum methylome with those in mouse and other marsupial species such as Tasmanian devil, kangaroos, and wallabies. Although the opossum methylome is similar to that of mouse during postnatal growth, it is not similar to that of other mammals when it comes to the age-related rise in methylation at target sites of polycomb repressive complex 2. Our immunohistochemical staining results add to the claim that PRC2 activity rises with mouse tissues age as we age, but in opossum tissues, remains stagnant. The human-opossum epigenetic clocks are expected to give opossum's attractiveness as a biological model.
Source link: https://europepmc.org/article/MED/35449380
Individuals with latent tuberculosis infection were regarded as a large reservoir of infectious tuberculosis infections. DNA methylation profiles were retrospectively found in an open-label controlled trial aimed at discovering short-course LTBI treatment regimens, and could help identify active TB from LTBI. The Infinium MethylationEPIC BeadChip array was used to determine genomewide DNA methylation levels for 15 people with LTBI who later developed active TB and 15 LTBI controls who remained healthy, as well as 15 LTBI controls who remained healthy. The potential value of the DNA methylation level as a diagnostic biomarker for distinguishing active disease in LTBI testing was shown in our preliminary results. IMPORTANCE Approximately a quarter of the world population had been infected with Mycobacterium tuberculosis, and around 5 to 10% of these people can live with active disease in their lifetimes. As a key component of the "end TB framework," preventive therapy has been shown to keep 60 to 90 percent of high-risk LTBIs from experiencing active disease. Before starting to investigate, developing new TB screening tools based on blood-based biomarkers that can help identify and rule out active TB from LTBI is a prerequisite. Pre- and post-TB diagnosis, we tried to identify potential DNA methylation diagnostic biomarkers by retrospectively detecting DNA methylation profiles. The combination of "cg02206980+ cg02214623+ cg12159502 + cg12321798" showed a sensitivity of 93. 3 percent and a specificity of 86. 6 percent, with a sensitivity of 86. 6 percent and a specificity of 86. 6 percent. The preliminary findings provided new insight into the determination of DNA methylation levels as a potential way to tell TB from LTBI.
Source link: https://europepmc.org/article/MED/35446152
According to a new analysis, the NRG1 rare variant frequency in Indonesian patients with HSCR is only 0. 9%. Methods This cross-sectional research revealed NRG1 type I, type II, and type III expressions in 20 patients with HSCR and ten control colons of 20 patients with HSCR and 10 control colons by real-time polymerase chain reaction. We treated the extracted gDNA from 16 HSCR patients' and 17 control colons with sodium bisulfate and analyzed the methylation pattern of NRG1 exon 1 in methylation-specific PCR for methylation studies. Results in the ganglionic colons were more restricted in comparison to the controls; however, only type I, II, and III expressions were significantly restricted; however, in the aganglionic colons, only type I and HRG1/HRG2 isoforms were significantly different from those in the controls.
Source link: https://europepmc.org/article/MED/35443634
We also predicted that EZH2 interacted with CRABP2, overexpression of CRABP2's promoted EZH2 expression, downplay of CRABP2's banned EZH2 expression, and co-imunoprecipitation assay confirmed their binding relationship. The SKOV3 and OVCAR3 cells were then incubated with pcDNA-CRABP2 alone, si-EZH2, and we discovered that si-EZH2 increased the activity of EZH2 expression, cell migration, and EMT manufacturer protein levels in a cell culture. We found that EZH2 could bind to DNMT1 in a new way, and that overexpression of EZH2 has blocked TRIM16 expression and brought down the EZH2 campaigned TRIM16 expression. Moreover, the promoter of TRIM16 is the CpG island, and ChIP assay results enriched DNMT1 on the promoter of TRIM16, while overexpression of EZH2 lowered the methylation rate, although EZH2 assay decreased the methylation. We discovered that si-EZH2 alone or in combination with si-TRIM16 incubated the SKOV3 cells, and we discovered that si-TRIM16 reversed the results of si-EZH2.
Source link: https://europepmc.org/article/MED/35442568
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