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Sobenin I.A.,Russian Academy of Medical Sciences | Sazonova M.A.,Russian Academy of Medical Sciences | Ivanova M.M.,Russian Academy of Medical Sciences | Zhelankin A.V.,Russian Academy of Medical Sciences | And 5 more authors.
PLoS ONE | Year: 2012

This study was undertaken to examine the association between the level of heteroplasmy for the mutation C3256T in human white blood cells and the extent of carotid atherosclerosis, as well as the presence of coronary heart disease (CHD), the major clinical manifestation of atherosclerosis. Totally, 191 participants (84 men, 107 women) aged 65.0 years (SD 9.4) were recruited in the study; 45 (24%) of them had CHD. High-resolution B-mode ultrasonography of carotids was used to estimate the extent of carotid atherosclerosis by measuring of the carotid intima-media thickness (cIMT). DNA samples were obtained from whole venous blood, and then PCR and pyrosequencing were carried out. On the basis of pyrosequencing data, the levels of C3256T heteroplasmy in DNA samples were calculated. The presence of the mutant allele was detected in all study participants; the level of C3256T heteroplasmy in white blood cells ranged from 5% to 74%. The highly significant relationship between C3256T heteroplasmy level and predisposition to atherosclerosis was revealed. In individuals with low predisposition to atherosclerosis the mean level of C3256T heteroplasmy was 16.8%, as compared to 23.8% in moderately predisposed subjects, and further to 25.2% and 28.3% in significantly and highly predisposed subjects, respectively. The level of C3256T heteroplasmy of mitochondrial genome in human white blood cells is a biomarker of mitochondrial dysfunction and risk factor for atherosclerosis; therefore, it can be used as an informative marker of genetic susceptibility to atherosclerosis, coronary heart disease and myocardial infarction. © 2012 Sobenin et al. Source


Bobryshev Y.V.,University of New South Wales | Karagodin V.P.,Institute for Atherosclerosis Research | Orekhov A.N.,Russian Academy of Medical Sciences
Cell and Tissue Biology | Year: 2013

Dendritic cells were discovered and recognized as antigen-presenting cells in 1973. Since then, a large volume of information has been accumulated showing the role of dendritic cells as a key element connecting the innate and adaptive immunity. Today, dendritic cells are considered to be dedicated sensors of the immune system that are capable of recognizing both antigen amounts and antigen persistence via complex mechanisms that involve decoding and integration of various signals received in a receptor-dependant manner. The tissue microenvironment plays an important role in the modulation of effector functions of dendritic cells, inducing either activation or suppression of immune reactions. Dendritic cells maintain homeostasis and are involved in a number of diseases, including infectious diseases and cancer. The presence of dendritic cells in arteries was reported in 1995, and, since then, the involvement of dendritic cells in atherogenesis has been evaluated. This review briefly describes the current knowledge of dendritic cells and their role in atherosclerosis. © 2013 Pleiades Publishing, Ltd. Source


Bobryshev Y.V.,University of New South Wales | Karagodin V.P.,Institute for Atherosclerosis Research | Orekhov A.N.,Institute for Atherosclerosis Research
Tsitologiya | Year: 2012

Dendritic cells were discovered and recognized as antigen-presenting cells in 1973. Since then, large volume of information has accumulated showing role of dendritic cells as a key element connecting the innate and adaptive immunity. Nowadays, dendritic cells are considered to be professional immune sensors capable of recognizing both antigen amounts and antigen persistence via complex mechanisms that involve decoding and integration of various signals received in a receptor-dependant manner. Tissue microenvironment plays an important role in the modulation of effector functions of dendritic cells leading either to activation or to suppression of immune reactions. Dendritic cells maintain the homeostasis and are involved in a number of diseases including infection diseases and cancer. The presence of dendritic cells in arteries has been reported in 1995. And since then the importance of dendritic cells in atherogenesis. is intensively studied. This review briefly described current knowledge on dendritic cells and their role in atherogenesis. Source


Sobenin I.A.,Institute of General Pathology and Pathophysiology | Myasoedova V.A.,Institute of General Pathology and Pathophysiology | Anisimova E.V.,Institute for Atherosclerosis Research | Pavlova X.N.,Institute for Atherosclerosis Research | And 11 more authors.
Current Pharmaceutical Design | Year: 2014

The phenomenon of blood serum atherogenicity was described as the ability of human serum to induce lipid accumulation in cultured cells. The results of recent two-year prospective study in asymptomatic men provided the evidence for association between the changes in serum atherogenicity and dynamics of carotid intima-media thickness progression. The present study was undertaken to test the hypothesis that blood serum atherogenicity and its changes in dynamics may be associated with accumulation of coronary calcium in subclinical atherosclerosis. It was performed in 782 CHD-free participants of The Heinz Nixdorf RECALL (Risk Factors, Evaluation of Coronary Calcium and Lifestyle) Study, in whom blood samples have been taken at the baseline and at the end of 5-year follow-up. Opposite to the previous findings, the changes in serum atherogenicity did not correlate neither with the extent of coronary artery calcification, nor with the changes in Agatston CAC score. There was a moderate but significant rise in serum atherogenicity after 5-year followup period, and the same dynamics was observed for Agatston CAC score, but not for convenient lipid-related risk factors. The absence of association of the changes in serum atherogenicity with the changes in Agatston CAC score, along with previous findings, provides a point of view that serum-induced intracellular cholesterol accumulation is not related to the processes of calcium deposition in arterial wall, since the last one reflects the progression of already existing subclinical atherosclerotic lesions. © 2014 Bentham Science Publishers. Source


Bobryshev Y.V.,Institute for Atherosclerosis Research | Karagodin V.P.,Institute for Atherosclerosis Research | Moisenovich M.M.,Institute for Atherosclerosis Research | Melnichenko A.A.,Institute for Atherosclerosis Research | Orekhov A.N.,Institute for Atherosclerosis Research
Tsitologiya | Year: 2013

It is generally recognized that the accumulation of lipids and immuno-inflammatory cells are early signs of atherosclerosis. In the present study, we have investigated the relationship between the deposition of lipids, of immuno-inflammatory cells and the expression of HLA-DR molecules (a marker of immune activation), the molecules of the class II of major histocompatibility complex (MHC) in diffuse thickening of the intima (DIT). Lipids, including triglycerides, cholesterol esters, free cholesterol and phospholipids were studied by chromatography, Oil Red O histochemisty, as well as by electron microscopic analysis. Immuno-inflammatory cells and the expression of HLA-DR were investigated by immunohistochemistry in consecutive section of the same tissue samples. It has been shown that the lipids were unevenly distributed in DIT. In juxtaluminal sublayer, lipids were detected both in the cytoplasm of intimal cells and extracellularly. In the juxtamedial musculoelastic sublayer of the intima, lipids were present predominantly along elastic fibers. The positive correlation between the presence of lipids and the expression of HLA-DR was revealed (r = 0.79; P < 0.001). Also, a positive correlation was found between the deposition of lipids and the number of immune-inflammatory cells, although correlations was different for different sublayers of the intima. In particular, the correlation between the deposition of lipids and immune-inflammatory cells in the juxtaluminal sublayer of the intima was higher (r = 0.99; P < 0.001) than in the juxtamedial musculoelastic layer (r = 0.28; P < 0.001). These data support the hypothesis that postulates that the accumulation of lipids in the intima is a key factor in the initiation of inflammatory reactions. At the pre-atherosclerotic stage of the development of this disease, earlier pathological processes associated with lipid-dependent activation of immune cells occur mainly in the juxtaluminal portion of the intima. Source

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