Stimulatory effect of fragments from transcribed region of ribosomal repeat on human peripheral blood lymphocytes

Вейко, Н. Н.; Калашникова, Е. А.; Кокаровцева, С. Н.; Kostyuk, Svetlana V.; Ermakov, A. N.; Ivanova, Saška; Ryazantseva, T. A.; Egolina, N. A.; Lyapunova, N. A.; Spitkovskii, D. M.

doi:10.1007/s10517-006-0384-9

Cited by 10 publications

(11 citation statements)

References 10 publications

(5 reference statements)

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“…TRrDNA content in ecDNA samples was established using quantitative hybridization [1,3]. ecDNA was separated from blood plasma, obtained from patients with atherosclerosis and arterial hypertension II grade (1)(2)(3)(4) or arterial hypertension without signs of atherosclerosis (5).…”

Section: Human Umbilical Vein Endothelial Cells (Huvec)mentioning

confidence: 99%

“…Accumulation of CG-DNA fragments in ecDNA is not indifferent for the cells, because they act as ligands interacting with TLR family proteins (TLR9) [3]. We previously showed that accumulation in ecDNA of one of repeating CG-DNA of human genome, transcribed region of ribosomal repeat (TRrDNA), containing binding sites for TLR9 can result in signifi cant lymphocyte activation accompanied by synthesis of proinfl ammatory cytokines [2]. In in vitro experiments, endogenous CG-DNAs accumulated in the blood of patients with cardiovascular diseases [1] reduced the rate of contraction of rat cardiomiocytes [7].…”

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confidence: 99%

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Extracellular DNA Affects NO Content in Human Endothelial Cells

et al. 2010

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Fragments of extracellular DNA are permanently released into the blood flow due to cell apoptosis and possible de novo DNA synthesis. To find out whether extracellular DNA can affect the synthesis of nitric oxide (NO), one of key vascular tone regulators, we studied in vitro effects of three artificial DNA probes with different sequences and 10 samples of extracellular DNA (obtained from healthy people and patients with hypertension and atherosclerosis) on NO synthesis in endothelial cell culture (HUVEC). For detection of NO in live cells and culture medium, we used a NO-specific agent CuFL penetrating into the cells and forming a fluorescent product FL-NO upon interaction with NO. Human genome DNA fragments affected the content of NO in endothelial cells; this effect depended on both the base sequence and concentration of DNA fragments. Addition of artificial DNA and extracellular DNA from healthy people into the cell culture in a low concentration (5 ng/ml) increased the detected NO concentration by 4-fold at most. Cytosine-guanine (CG)-rich fragment of the transcribed sequence of ribosomal repeat was the most powerful NO-inductor. The effect of DNA fragments on NO synthesis was comparable with that of low doses of oxidizing agents, H(2)O(2) and 17β-estradiol. Extracellular DNA samples obtained from patients with hypertension and atherosclerosis decreased NO content in cells and medium by 1.3-28 times compared to the control; the effect correlated with the content of CG-rich sequences.

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Section: Human Umbilical Vein Endothelial Cells (Huvec)mentioning

confidence: 99%

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confidence: 99%

Extracellular DNA Affects NO Content in Human Endothelial Cells

et al. 2010

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“…Based on the conclusions made from the results of our studies of cfDNA properties, we determined the most significant cfDNA parameters, which can evoke biological responses in different cell types: Elevated GC-rich DNA content of the cfDNA, in particular, elevated ribosomal DNA (rDNA) content [ 14 , 52 ]. Increased content of oxidized DNA fragments [ 15 , 53 ].…”

Section: Methodsmentioning

confidence: 99%

“…Elevated GC-rich DNA content of the cfDNA, in particular, elevated ribosomal DNA (rDNA) content [ 14 , 52 ].…”

Section: Methodsmentioning

confidence: 99%

Changes of KEAP1/NRF2 and IKB/NF‐κB Expression Levels Induced by Cell‐Free DNA in Different Cell Types

Kostyuk

Porokhovnik

Ershova

et al. 2018

Oxidative Medicine and Cellular Longevity

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Cell-free DNA (cfDNA) is a circulating DNA of nuclear and mitochondrial origin mainly derived from dying cells. Recent studies have shown that cfDNA is a stress signaling DAMP (damage-associated molecular pattern) molecule. We report here that the expression profiles of cfDNA-induced factors NRF2 and NF-κB are distinct depending on the target cell's type and the GC-content and oxidation rate of the cfDNA. Stem cells (MSC) have shown higher expression of NRF2 without inflammation in response to cfDNA. In contrast, inflammatory response launched by NF-κB was dominant in differentiated cells HUVEC, MCF7, and fibroblasts, with a possibility of transition to massive apoptosis. In each cell type examined, the response for oxidized cfDNA was more acute with higher peak intensity and faster resolution than that for nonoxidized cfDNA. GC-rich nonoxidized cfDNA evoked a weaker and prolonged response with proinflammatory component (NF-κB) as predominant. The exploration of apoptosis rates after adding cfDNA showed that cfDNA with moderately increased GC-content and lightly oxidized DNA promoted cell survival in a hormetic manner. Novel potential therapeutic approaches are proposed, which depend on the current cfDNA content: either preconditioning with low doses of cfDNA before a planned adverse impact or eliminating (binding, etc.) cfDNA when its content has already become high.

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“…3 The rDNA fragments activate immune system cells, and this interaction is accomplished by the binding of the CpG-rich rDNA motifs with the "toll"-like receptors (TLR9). 4 Since the cardiomyocytes express TLR9, 5 we would assume that for patients with AMI the CpG-rich fragments of the cfDNA influence myocardial cell operation. To examine the hypothesis, we studied the effect of different fragments of human DNA on the frequency of contraction of the electrically paced neonatal rat ventricular myocytes in culture.…”

Section: Introductionmentioning

confidence: 99%

Effect of Cell‐Free DNA of Patients with Cardiomyopathy and rDNA on the Frequency of Contraction of Electrically Paced Neonatal Rat Ventricular Myocytes in Culture

Bulicheva

Fidelina

Mkrtumova

et al. 2008

Annals of the New York Academy of Sciences

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There is evidence that infarcted myocardium contributes to the increase of cell-free DNA levels (cfDNA). We studied the effect of different human DNA fragments on the rate of contraction of the electrically paced neonatal rat ventricular myocytes in culture (spontaneously hypertensive line SHR). AT-rich fragments of the human satellite 3 tandem repeat (1q12 region) at a concentration of 1 ng/mL increase the frequency of cardiomyocyte contractions by 2-2.5 times. GC-rich fragments of the rDNA at 0.5 ng/mL decrease the cardiomyocyte contraction frequency by 1.5-2 times. The serum cfDNA of patients with acute myocardial infarction decreases the frequency of the contraction of cardiomyocytes proportionally to the amount of the rDNA fragments it contains. The rDNA effect is similar to the E. coli DNA effect and is presumably being realized through TLR9. In the presence of the inhibitor of these receptors, rDNA operates the same way as the fragment of the satellite 3-increasing the frequency of the cardiomyocyte contractions. Accumulation of the GC-rich fragments of the cfDNA in the blood of the AMI patients might have an influence on the contractile function of myocardial cells.

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Stimulatory effect of fragments from transcribed region of ribosomal repeat on human peripheral blood lymphocytes

Cited by 10 publications

References 10 publications

Extracellular DNA Affects NO Content in Human Endothelial Cells

Extracellular DNA Affects NO Content in Human Endothelial Cells

Changes of KEAP1/NRF2 and IKB/NF‐κB Expression Levels Induced by Cell‐Free DNA in Different Cell Types

Effect of Cell‐Free DNA of Patients with Cardiomyopathy and rDNA on the Frequency of Contraction of Electrically Paced Neonatal Rat Ventricular Myocytes in Culture

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