Alu repetitive sequence CpG methylation changes in burn scars

Meevassana, Jiraroch; Serirodom, Siwat; Prabsattru, Piyawan; Boonsongserm, Papatson; Kamolratanakul, Supitcha; Siritientong, Tippawan; Mutirangura, Apiwat; Angspatt, Apichai

doi:10.1016/j.burns.2021.10.002

Cited by 4 publications

(1 citation statement)

References 40 publications

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“…Genome-wide hypomethylation also occurs when cells are exposed to hazardous environments, such as smoke, benzene, burns, and oxidative stress (55)(56)(57)(58). Environmental hazards are also associated with DNA damage, which leads to demethylation and repair, and HMGB1 release (59,60).…”

Section: Causes Of Global Hypomethylationmentioning

confidence: 99%

Genome wide hypomethylation and youth-associated DNA gap reduction promoting DNA damage and senescence-associated pathogenesis

Watcharanurak

Mutirangura

2022

Preprint

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Background: Age-associated epigenetic alteration is the underlying cause of DNA damage in aging cells. Two types of youth-associated DNA-protection epigenetic marks, global methylation, and youth-associated genomic stabilization DNA gap (youth-DNA-gap) reduce when cell ages. The epigenomic mark reduction promotes DNA damage and accelerates aging hallmarks. While DNA hypomethylation destabilizes DNA by several mechanisms, the DNA sequence around the youth-DNA-gap is hypermethylated. Therefore, the genomic instability mechanisms underlying DNA hypomethylation and youth-DNA-gap reduction are linked. Results: DNA gap prevents DNA damage by relieving the torsion forces caused by a twisted wave during DNA strand separation by transcription or replication. When the cells begin to age, hypomethylation and youth-DNA-gap reduction can occur as consequences of the efflux of intranuclear HMGB1. The methylated DNA gaps are formed by several proteins. Box A of HMGB1 possesses a molecular scissor role in producing youth-DNA-gaps. So the lack of a gap-producing role of HMGB1 results in a youth-DNA-gap reduction. The histone deacetylation role of SIRT1, an aging prevention protein, prevents DNA ends of youth-DNA-gaps from being recognized as pathologic DNA breaks. Youth-DNA-gaps are methylated and determined genome distribution by AGO4, an effector protein in RNA-directed DNA methylation. The lack of intranuclear HMGB1 promotes global hypomethylation due to two subsequent mechanisms. First is the loss of AGO4-methylating DNA. The other is the accumulation of DNA damage due to lacking HMGB1-produced DNA gap promoting DNA demethylation while undergoing DNA repair. DNA torsion due to youth-DNA-gap reduction increases DNA damage and, consequently, the DNA damage response (DDR). Persistent DDR promotes cellular senescence. Accumulating senescent cells leads to the deterioration of the structure and function of the human body. Rejuvenating DNA (RED) by adding DNA protection epigenetic marks using genomic stability molecule (GEM) such as box A of HMGB1 increases DNA durability, limits DNA damage, rejuvenates senescence cells, and improves organ structure and function deterioration due to aging. Conclusion: Reducing youth-associated epigenetic marks is a degenerative diseases' primary molecular pathogenesis mechanism. REDGEM is a new therapeutic strategy inhibiting the upstream molecular aging process that will revolutionize the treatment of DNA damage or age-associated diseases and conditions.

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Section: Causes Of Global Hypomethylationmentioning

confidence: 99%

Genome wide hypomethylation and youth-associated DNA gap reduction promoting DNA damage and senescence-associated pathogenesis

Watcharanurak

Mutirangura

2022

Preprint

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Targeting DNA methylation and demethylation in diabetic foot ulcers

Deng

et al. 2023

Journal of Advanced Research

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Breast Cancer Sera Changes in Alu Element Methylation Predict Metastatic Disease Progression

Denariyakoon¹,

Puttipanyalears²,

Chatamra³

et al. 2022

CDP

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Background/Aim: During metastatic disease development, the cancer-immune system crosstalk induces epigenetic modifications to immune cells, impairing their functions. Recently, Alu elements methylation changes were widely studied in terms of early cancer detection. This study aimed to demonstrate in vitro Alu element methylation changes in peripheral immune cells in a metastatic setting and examine their prognostic values in metastatic breast cancer. Materials and Methods: Sera from sixteen metastatic cancer patients and sixteen healthy participants were obtained and used to culture normal peripheral immune cells. After 48 h of incubation, the percentage and pattern of Alu element methylation were examined for clinical relevance. Results: We found that the Alu element hypomethylation was affected by age in the cancer group. Intriguingly, a decrease in Alu element methylation was found in patients with early progressive disease. Moreover, an increase in unmethylated cytosine (mCuC) loci was related to the poorer prognosis group. Accordingly, the decrease in Alu element methylation and the increase in mCuC loci pattern in peripheral immune cells correlated with poorer prognosis and early progression in metastatic breast cancer. Conclusion: Alu element hypomethylation in immune cells and their increased mCuC foci were related to the early progression of breast cancer. These warrant the use of Alu element methylation changes for diagnostic and therapeutic purposes in breast cancer.

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Alu repetitive sequence CpG methylation changes in burn scars

Cited by 4 publications

References 40 publications

Genome wide hypomethylation and youth-associated DNA gap reduction promoting DNA damage and senescence-associated pathogenesis

Genome wide hypomethylation and youth-associated DNA gap reduction promoting DNA damage and senescence-associated pathogenesis

Targeting DNA methylation and demethylation in diabetic foot ulcers

Breast Cancer Sera Changes in Alu Element Methylation Predict Metastatic Disease Progression

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