Dysregulation of apoptotic death in the pathogenesis of virus-induced cytogenetic instability of blood lymphocytes

Ryazantseva, N. V.; Новицкий, В. В.; Жукова, О. Б.; Radzivil, T. T.; Михеев, С. Л.; Чечина, О. Е.; Зима, А. П.; Shilov, B. V.

doi:10.1007/s10517-006-0233-x

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…It implies binding of TNFR1 with the corresponding ligand and formation of a complex between intracellular areas of the receptor and adaptor protein TRADD (TNFR-associated death domain). The latter induces oligomerization of caspase-8 and its autoproteolysis [1,2,7]. Caspase-8 affects effector proteases (caspases 3 and 7), which activate caspase 6 cleaving nuclear mitotic apparatus protein and mediating shrinkage and fragmentation of the nucleus [10].…”

Section: Resultsmentioning

confidence: 99%

Modulation of apoptosis of mononuclear cells under conditions of oxidative stress

et al. 2008

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We studied mitochondrial and type 1 tumor necrosis factor-a receptor (TNFR1)-mediated pathways triggering the apoptotic program in mononuclear cells under conditions of oxidative stress. Intensification of intracellular production of reactive oxygen forms is accompanied by an increase in the number of annexin-positive TNFRI-presenting cells and mononuclear cells with reduced mitochondrial transmembrane potential in case of induction of oxidative stress with 1 mM H2O2 in vitro and in patients with pneumonia.

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Section: Resultsmentioning

confidence: 99%

Modulation of apoptosis of mononuclear cells under conditions of oxidative stress

et al. 2008

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“…HBV-DNA integration into the host cell genome can lead to increased frequencies of chromosomal instability and genetic recombinations (6). Cytogenetic instability of immune system cells in chronic viral infections has been associated with inhibition of the DNA excision repair system and disregulation of apoptosis in target cells (7). …”

Section: Introductionmentioning

confidence: 99%

Role of p53 codon 72 polymorphism in chromosomal aberrations and mitotic index in patients with chronic hepatitis B

Akbas

Yalçın

Isi

et al. 2012

Braz J Med Biol Res

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Polymorphisms of the p53 gene, which participates in DNA repair, can affect the functioning of the p53 protein. The Arg and Pro variants in p53 codon 72 were shown to have different regulation properties of p53-dependent DNA repair target genes that can affect various levels of cytogenetic aberrations in chronic hepatitis B patients. The present study aimed to examine the frequency of chromosomal aberrations and the mitotic index in patients with chronic hepatitis B and their possible association with p53 gene exon 4 codon 72 Arg72Pro (Ex4+119 G>C; rs1042522) polymorphism. Fifty-eight patients with chronic hepatitis B and 30 healthy individuals were genotyped in terms of the p53 gene codon 72 Arg72Pro polymorphism by PCR-RFLP. A 72-h cell culture was performed on the same individuals and evaluated in terms of chromosomal aberrations and mitotic index. A high frequency of chromosomal aberrations and low mitotic index were detected in the patient group compared to the control group. A higher frequency of chromosomal aberrations was detected in both the patient and the control groups with a homozygous proline genotype (13 patients, 3 control subjects) compared to patients and controls with other genotypes [Arg/Pro (38 patients, 20 control subjects) and Arg/Arg (7 patients, 7 control subjects)]. We observed an increased frequency of cytogenetic aberrations in patients with chronic hepatitis B. In addition, a higher frequency of cytogenetic aberrations was observed in p53 variants having the homozygous proline genotype compared to variants having other genotypes both in patients and healthy individuals.

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Role of protein kinases JNK and p38 in regulation of mononuclear leucocytes apoptosis in oxidative stress

Chasovskikh¹

2008

Bûll. sib. med.

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Programmed cell death of peripheral blood mononuclear leucocytes taken from healthy donors and cultivated with various concentration of Н2О2, selective inhibitors of JNK (SP600125), 38 (ML3403) and in case of pneumonia was investigated. Intensification of intracellular production of reactive oxy р МАРК - gen species was accompanied by the increase in number of apoptotic and TNFR1-presented cells and mononuclears with reduced value of mitochondrial transmembrane potential in a case of oxidative stress induction with 1 mM hydrogen peroxide and in blood taken from patients with pneumonia. Action of inhibitors SP600125 and ML3403 in vitro in oxidative stress conditions prevents the increase in number of annexin- positive mononuclear cells, that confirms the participation of JNK and 38 -kinases in mechanisms of oxidative stress-mediated apoptosis dysregulation.

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Dysregulation of apoptotic death in the pathogenesis of virus-induced cytogenetic instability of blood lymphocytes

Cited by 3 publications

References 8 publications

Modulation of apoptosis of mononuclear cells under conditions of oxidative stress

Modulation of apoptosis of mononuclear cells under conditions of oxidative stress

Role of p53 codon 72 polymorphism in chromosomal aberrations and mitotic index in patients with chronic hepatitis B

Role of protein kinases JNK and p38 in regulation of mononuclear leucocytes apoptosis in oxidative stress

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