Changes in <i>DNMT1</i> expression as a marker of epigenetic regulation disturbanses in multiple sclerosis patients DOI

Evgenia A. Tsymbalova,

Ekaterina А. Chernyavskaya,

Darja Е. Ryzhkova

et al.

Medical academic journal, Journal Year: 2024, Volume and Issue: 23(3), P. 41 - 53

Published: March 29, 2024

BACKGROUND: Multiple sclerosis is a chronic neurodegenerative autoimmune disease characterized by the presence of foci inflammation and demyelination in central nervous system. The initiation pathological processes multiple caused complex interaction genetic factors, unfavorable environmental factors epigenetic influences. Progressive neurological symptoms axonal conduction disorders, death neurodestruction lead to significant decreased patients’ quality life disability. search for new markers improve diagnostic therapeutic methods, including taking into account background interactions, an urgent task. AIM: work was aimed study changes DNMT1 mRNA expression patients with different duration, analyze methylation promoter, compare level homocysteine content blood, polymorphic variants genes coding key folate cycle enzymes. MATERIALS AND METHODS: peripheral mononuclear blood cells assessed reversed transcription followed polymerase chain reaction. Fluorescent reaction methyl-sensitive analysis high-resolution melting curves used promoter. determined chemiluminescence immunoassay. real-time genotyping polymorphism genes; fluorescent probes LNA modifications were discriminate alleles. RESULTS: It has been shown that patients, those at onset disease, significantly lower than control group. No relationship found between decrease promoter methylation. Strong positive combined effects genotypes MTR A2756G MTHFR C677T on have shown. These findings suggest genetically features metabolism may contribute disruption regulation sclerosis. CONCLUSIONS: obtained results indicate promise research identifying causing Studying mechanisms contribution pathogenesis could be one possible ways approaches.

Language: Английский

Biological mechanisms underlying depression, epigenetics and their interplay (Review) DOI Creative Commons
Τhanasis Mitsis, Eleni Papakonstantinou, Dimitriοs Vlachakis

et al.

Deleted Journal, Journal Year: 2023, Volume and Issue: 3(1)

Published: June 7, 2023

Depression is a prevalent mood disorder that heavily affects the quality of life affected individuals. The pathogenesis depression relatively complex, with existing hypotheses focusing on alterations in monoamine signaling, dysfunction hypothalamus‑pituitary‑adrenal glands axis, and deregulated immune response. Moreover, effectiveness currently used pharmacotherapy, which mostly based hypothesis, not satisfactory. study epigenetics, i.e., heritable, stable structural biochemical chromosome are associated DNA sequence alterations, may help to elucidate molecular mechanisms underlying response patients antidepressants. Epigenetic mechanisms, such as methylation, histone modifications regulation by non‑coding RNAs appear affect disease play crucial role functions Therefore, research influence epigenetics prove be fruitful. present review aims accumulate all known information regarding biological depression,

Language: Английский

Citations

3
S100A6 participates in initiation of autoimmune encephalitis and is under epigenetic control DOI Creative Commons
Chih‐Hsiang Lin, Sung‐Chou Li, Ming‐Hong Lin

et al.

Brain and Behavior, Journal Year: 2023, Volume and Issue: 13(3)

Published: Feb. 7, 2023

Abstract Introduction Autoimmune encephalitis (AE) is caused by autoantibodies attacking neuronal cell surface antigens and/or synaptic antigens. We previously demonstrated that S100A6 was hypomethylated in patients with AE and it promoted B lymphocyte infiltration through the simulated blood–brain barrier (BBB). In this study, we focused on epigenetic regulation of , process which affects infiltration, therapeutic potential antibodies. Methods enrolled collected serum from 10 healthy control (HC) subjects. Promoter methylation 5‐azacytidine treatment assays were conducted to observe . The effect lymphocytes analyzed using an adhesion assay leukocyte transendothelial migration (LTEM) assay. A LTEM also used compare effects HCs, patients, recombinant protein, antibodies lymphocytes. Result promoter confirmed regulated DNA methylation. study addition enhanced between a BBB endothelial line concentration‐dependent manner. showed as well S100A6, could be attenuated Conclusion clarified under helped adhere infiltrate layer, counteracted Therefore, profile marker activity AE, countering may target for AE.

Language: Английский

Citations

2
Epigenetics and multifactorial diseases DOI Creative Commons

N. V. Vokhmyanina

Russian Journal for Personalized Medicine, Journal Year: 2024, Volume and Issue: 3(6), P. 42 - 49

Published: Jan. 16, 2024

At present, epigenetics is being studied in detail and actively, the significance of development multifactorial diseases has been determined. In this regard, a large number publications have recently appeared that analyze results studies using epigenetic markers. The obtained promising indicate possibility early detection prediction many diseases. This review briefly outlines theoretical foundations mechanisms. participation formation pathology considered on example celiac disease, multiple sclerosis cardiovascular diseases, confirmed by identified

Language: Английский

Citations

0
Incorporation of DNA methylation profiling into the cytopathology laboratory DOI
Gloria H. Sura, Leomar Y. Ballester

Cancer Cytopathology, Journal Year: 2024, Volume and Issue: 132(9), P. 543 - 546

Published: March 15, 2024

Language: Английский

Citations

0
Changes in <i>DNMT1</i> expression as a marker of epigenetic regulation disturbanses in multiple sclerosis patients DOI

Evgenia A. Tsymbalova,

Ekaterina А. Chernyavskaya,

Darja Е. Ryzhkova

et al.

Medical academic journal, Journal Year: 2024, Volume and Issue: 23(3), P. 41 - 53

Published: March 29, 2024

BACKGROUND: Multiple sclerosis is a chronic neurodegenerative autoimmune disease characterized by the presence of foci inflammation and demyelination in central nervous system. The initiation pathological processes multiple caused complex interaction genetic factors, unfavorable environmental factors epigenetic influences. Progressive neurological symptoms axonal conduction disorders, death neurodestruction lead to significant decreased patients’ quality life disability. search for new markers improve diagnostic therapeutic methods, including taking into account background interactions, an urgent task. AIM: work was aimed study changes DNMT1 mRNA expression patients with different duration, analyze methylation promoter, compare level homocysteine content blood, polymorphic variants genes coding key folate cycle enzymes. MATERIALS AND METHODS: peripheral mononuclear blood cells assessed reversed transcription followed polymerase chain reaction. Fluorescent reaction methyl-sensitive analysis high-resolution melting curves used promoter. determined chemiluminescence immunoassay. real-time genotyping polymorphism genes; fluorescent probes LNA modifications were discriminate alleles. RESULTS: It has been shown that patients, those at onset disease, significantly lower than control group. No relationship found between decrease promoter methylation. Strong positive combined effects genotypes MTR A2756G MTHFR C677T on have shown. These findings suggest genetically features metabolism may contribute disruption regulation sclerosis. CONCLUSIONS: obtained results indicate promise research identifying causing Studying mechanisms contribution pathogenesis could be one possible ways approaches.

Language: Английский

Citations

0