The effect of low-intensity electromagnetic irradiation with a frequency of 1 GHz on the content of the components of the IL1/TOLL signaling pathway and NF-kB in mononuclear cells of whole blood

2017 ◽  
Vol XII (2) ◽  
Author(s):  
I. Terekhov ◽  
V. Nikiforov ◽  
S. Bondar ◽  
N. Bondar ◽  
A. Voevodin
2016 ◽  
Vol 10 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Логаткина ◽  
A. Logatkina ◽  
Бондарь ◽  
S. Bondar ◽  
Терехов ◽  
...  

Molecular indicators reflecting the states of stress-limiting systems of mononuclear leucocytes in the blood, as well as the effects of low-intensive microwave radiation in patients with coronary artery disease were studied. The work it was evaluated the content in mononuclear leucocytes whole blood of components PI3P/AKT/mTOR/p70S6K1 of signaling pathway, heat shock proteins (HSP27, HSP70, HSP90), the concentra-tion of antioxidants and peroxides depending on the level of phosphorylation of the terminal protein kinase MAPK/SAPK of signaling pathway – p38. The results of the study. It was revealed the dependence of a level of studied factors from the degree of phosphorylation p38 in patients with coronary heart disease. It was defined the 38 p sensitivity to the effects of low-intensity microwave radiation, it is manifested by increased level of phosphorylation in the irradiated cul-tures. This study revealed the sensitivity to low-intensity microwave irradiation of content in the mononuclear cells phosphorylated forms of the protein kinases AMPK, AKT1, p70S6K1, as well as the antioxidant status and protein of p53-dependent initial content in the cell phosphorylated form p38. It was shown a possibility of microwave radiation to reduce the content in the cells of the protein kinase and p70 ACT more pronounced at high levels of phosphorylation p38.


2021 ◽  
Vol 23 (1) ◽  
Author(s):  
M. Badii ◽  
O. I. Gaal ◽  
M. C. Cleophas ◽  
V. Klück ◽  
R. Davar ◽  
...  

Abstract Objectives Hyperuricemia is a metabolic condition central to gout pathogenesis. Urate exposure primes human monocytes towards a higher capacity to produce and release IL-1β. In this study, we assessed the epigenetic processes associated to urate-mediated hyper-responsiveness. Methods Freshly isolated human peripheral blood mononuclear cells or enriched monocytes were pre-treated with solubilized urate and stimulated with LPS with or without monosodium urate (MSU) crystals. Cytokine production was determined by ELISA. Histone epigenetic marks were assessed by sequencing immunoprecipitated chromatin. Mice were injected intraarticularly with MSU crystals and palmitate after inhibition of uricase and urate administration in the presence or absence of methylthioadenosine. DNA methylation was assessed by methylation array in whole blood of 76 participants with normouricemia or hyperuricemia. Results High concentrations of urate enhanced the inflammatory response in vitro in human cells and in vivo in mice, and broad-spectrum methylation inhibitors reversed this effect. Assessment of histone 3 lysine 4 trimethylation (H3K4me3) and histone 3 lysine 27 acetylation (H3K27ac) revealed differences in urate-primed monocytes compared to controls. Differentially methylated regions (e.g. HLA-G, IFITM3, PRKAB2) were found in people with hyperuricemia compared to normouricemia in genes relevant for inflammatory cytokine signaling. Conclusion Urate alters the epigenetic landscape in selected human monocytes or whole blood of people with hyperuricemia compared to normouricemia. Both histone modifications and DNA methylation show differences depending on urate exposure. Subject to replication and validation, epigenetic changes in myeloid cells may be a therapeutic target in gout.


2014 ◽  
Vol 10 (8) ◽  
pp. e1003807 ◽  
Author(s):  
Priscilla Ambrosi ◽  
Juan Sebastian Chahda ◽  
Hannah R. Koslen ◽  
Hillel J. Chiel ◽  
Claudia Mieko Mizutani

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