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Aberrant Methylation - Europe PMC

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Last Updated: 15 November 2022

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Aberrant elevation of FTO levels promotes liver steatosis by decreasing the m6A methylation and increasing the stability of SREBF1 and ChREBP mRNAs.

The most common chronic liver disease worldwide, according to previous studies, there was an association of fat mass and obesity-related with nonalcoholic fatty liver disease. We found that a decrease in N6-methyladenosine RNA methylation in mice fed a high-fat diet was followed by a rise in FTO expression. Both master lipogenic transcription factors, methylating m6A sites, according to Mechanistical studies, FTO could stabilize the mRNAs of sterol regulatory element binding factor 1 and carbohydrate responsive element binding protein. Insulin could promote FTO transcription by a process involving intranuclear insulin receptor beta, while the FTO's shutdown delayed insulin's lipogenic effect. Thus, our report demonstrated that FTO is playing a vital role in both the insulin-regulated hepatic lipogenesis and the pathogenesis of NAFLD, as well as a potential treatment for NAFLD.

Source link: https://europepmc.org/article/MED/36352530


Pan-cancer landscape of aberrant DNA Methylation across childhood Cancers: Molecular Characteristics and Clinical relevance.

Pan-cancer DNAm testing has investigated the potential common causes of tumorigenesis. However, these pan-cancer reviews primarily focused on adult cancers rather than pediatric cancers, rather than pediatric cancers, which can have distinctive pathology and treatment responses. We performed a pan-cancer analysis of genome-wide DNA in over 2,000 samples from nine pediatric cancers to help define the pediatric cancer genome. 77. 65% of adults with adult cancers had DNA mutations, one of many. We identified 54 shared DMCs in nine pediatric cancers, which were also present in at least one adult cancer type. Interestingly, SDMCs may have a direct influence on patient survival not only in the nine pediatric cancers that were used to identify SDMCs, but also in other untested pediatric cancers. We also suggest the use of SDMCs as biomarkers of pediatric cancer diagnosis.

Source link: https://europepmc.org/article/MED/36348462


Aberrant DNA methylation and expression of EYA4 in gastric cardia intestinal metaplasia.

Herein, we wanted to provide an overview of the epidemiological evidence for gastric cardiac IM and determining the role of EYA transcriptional coactivator and phosphatase 4 as an epigenetic biomarker for gastric cardiac IM. Gastric cardiac IM was present in 14. 1% of participants, and was more prevalent among older than younger participants. Pyrosequencing revealed that IM tissues had significantly higher DNA methylation levels in the EYA4 gene than normal tissues. IM and absence in intraepithelial neoplasia tissues were reduced in IM and absent in intraepithelial neoplasia tissues in comparison to normal tissues, according to analysis. Conclusions: Gastric heart IM detection rates rise with age and are in men at a higher rate. Our results reveal the vital role of promoter hypermethylation and downregulation of EYA4 in gastric cardiac IM growth.

Source link: https://europepmc.org/article/MED/36348610


Meta-analysis of DNA methylation datasets shows aberrant DNA methylation of thyroid development or function genes in Down syndrome.

Background In Down syndrome, there is a high risk of congenital hypothyroidism and hypothyroidism early in life. The etiology of CH and early SH in DS remains uncertain. We hypothesized that CH and early SH could be attributed to epigenetically triggered transcriptional downregulation of thyroid-related genes as a result of promoter region hypermethylation. Methods We extracted whole blood DNA methylation profiles of DS and non-DS individuals from four independent Illumina array-based databases. Differential methylation of thyroid-related genes is not responsible for CH and early SH in DS, not caused by a chromosome abnormality. Since epigenetic control is fluid, we hypothesize the observed thyroid-related gene DNAm changes, which may be a rescue mechanism in an attempt to normalize the thyroid phenotype through epigenetic upregulation of thyroid-related genes. Although this report provides interesting insights, the precise source of CH and early SH in DS remains unknown.

Source link: https://europepmc.org/article/MED/36326208


Aberrant DNA and RNA Methylation Occur in Spinal Cord and Skeletal Muscle of Human SOD1 Mouse Models of ALS and in Human ALS: Targeting DNA Methylation Is Therapeutic.

Mutant hSOD1 mutant mice had increased DNA methyltransferase enzyme activity in spinal cord and skeletal muscle, as well as elevated 5-methylcytosine levels. In mice, mice that were mouse grew in spinal cord MNs and skeletal muscle satellite cells. In spinal cord nuclear and chromatin bound extracts of the different hSOD1 mouse strains, there were significant rises in DNA methyltransferase-1 and DNA methyltransferase-3A values. In mouse spinal cord, methylation was either increased or decreased in mouse spinal cord according to the hSOD1-G93A model, while fat mass and obesity-related protein was depleted, and methyltransferase-like protein 3 was added in spinal cord and skeletal muscle. Human ALS spinal cord with nuclear 5 millionC had elevated numbers of MNs and interneurons, and motor cortex had increased 5mC-positive neurons, while 6 millionA was severely depleted. Treatment of hSOD1-G93A mice with a DNMT inhibitor improved motor performance and increased lifespan by 25%.

Source link: https://europepmc.org/article/MED/36359844


The new mechanism of cognitive decline induced by hypertension: High homocysteine-mediated aberrant DNA methylation.

Hypertension-induced cognitive decline with the increase of hypertension-induced cognitive decline. The causes of cognitive impairment caused by hypertension include cerebral blood flow perfusion disruption, white and gray matter injury with blood-brain barrier disruption, neuroinflammation and amyloid deposition, and blood pressure instability. High homocysteine is an independent risk factor for hypertension that also raises the risk of developing early cognitive impairment. Patients with cognitive impairment caused by hypertension's hypertension are getting more frequent by Homocysteine. Methionine has been shown to cause hypertension in mice, according to research. These findings, taken together, show that DNA methylation regulates cognitive dysfunction in patients with hypertension. Early diagnosis, intervention, and prevention of more cognitive deficits caused by hypertension will be beneficial for early detection, treatment, and prevention of further cognitive defects related to hypertension-induced cognitive impairment.

Source link: https://europepmc.org/article/MED/36352848


Deciphering the role of aberrant DNA methylation in NAFLD and NASH.

The global incidence of nonalcoholic fatty liver disease is increasing incessantly, and it is becoming the most common cause of chronic and end stage liver disease. Improved DNA methylation pattern, according to emerging evidence, is a key determinant of NAFLD pathogenesis. DNA methylation patterns can be altered in a reversible manner by environmental and lifestyle causes, which manifests as changes in gene expression. We hope to emphasize the role of DNA methylation in the establishment and progression of NAFLD in this article. The development of novel diagnostic, prognostic, and therapeutic strategies based on DNA methylation signatures and modifiers has also been investigated.

Source link: https://europepmc.org/article/MED/36299516

* 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