Institute of General Pathology and Pathophysiology RAMS

Moscow, Russia

Institute of General Pathology and Pathophysiology RAMS

Moscow, Russia
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Gruden M.A.,P K Anokhin Institute Of Normal Physiology Rams | Sewell R.D.E.,University of Cardiff | Yanamandra K.,Umeå University | Davidova T.V.,Institute of General Pathology and Pathophysiology RAMS | And 4 more authors.
Journal of Neuroimmunology | Year: 2011

The aim was to ascertain any possible linkage between humoral immune responses to principal biomarkers (α-synuclein monomers, its toxic oligomers or fibrils, dopamine and S100B) and cellular immunity in Parkinson's disease development. There were elevated autoantibody titers to α-synuclein monomers, oligomers plus fibrils in 72%, 56%, and 17% of Parkinsonian patients respectively with a 5-year disease duration. Additionally, there were increased titers to dopamine and S100B (96% and 89%) in the 5-year patient group. All of these values subsided in 10-year sufferers.Furthermore, CD3+, CD4+, CD8+ T-lymphocyte and B-lymphocyte subsets declined in the patient cohort during Parkinsonism indicating disease associated reductions in these lymphocyte subsets. © 2010 Elsevier B.V.

Davydov D.M.,Moscow State University | Lobanov A.V.,RAS Shemyakin Ovchinnikov Institute of Bioorganic Chemistry | Morozov S.G.,Institute of General Pathology and Pathophysiology RAMS | Gribova I.E.,Institute of General Pathology and Pathophysiology RAMS | Murashev A.N.,RAS Shemyakin Ovchinnikov Institute of Bioorganic Chemistry
Physiology and Behavior | Year: 2015

The importance of certain neurotrophic proteins found in maternal blood and milk for breastfed infants has remained ambiguous. This study was conducted to present evidence of the impact of an induced deficit of active S100B protein on neonate development. Newborn mice from two groups of mothers, immunized or sham-immunized against S100B, were subjected to various behavioral tests, and the development of their morphological characteristics was recorded from birth until weaning. Morphological problems, including weight gain and fur coating, a delay in the maturation of neurobehavioral systems and a deficit in neuromotor functions, including visual abilities, somato-sensory and posture reactions, muscular strength, locomotion, and fear/orienting processes, were observed in pups of immunized mothers. The S100B protein of external or internal origin in infants may be considered to be a specific factor that determines neuro- and morphological development and a risk-avoidance ('homeward-bent' or fearful) phenotype. The suppression of activity of the S100B protein results in a slower neonatal development and the formation of a risk-tolerant (fearless) phenotype of the offspring. This study thus considers the mechanism of neuroplastic regulation on the extent of sensation-seeking or risk-taking (homeless-like or fearless) and sensation- or risk-avoidance (home-bound or fearful) features in individual phenotypes. © 2014 Elsevier Inc.

Kolikova J.,University of Helsinki | Afzalov R.,University of Helsinki | Surin A.,University of Helsinki | Surin A.,Institute of General Pathology and Pathophysiology RAMS | And 3 more authors.
Cell Calcium | Year: 2011

Neuronal ceroid lipofuscinoses (NCLs) are a group of genetic childhood-onset progressive brain diseases characterized by a decline in mental and motor capacities, epilepsy, visual loss and premature death. Using patch clamp, fluorescence imaging and caged Ca 2+ photolysis, we evaluated the mechanisms of neuronal Ca 2+ clearance in Cln8 mnd mice, a model of the human NCL caused by mutations in the CLN8 gene. In Cln8 mnd hippocampal slices, Ca 2+ clearance efficiency in interneurons and, to some extent, principal neurons declined with age. In cultured Cln8 mnd hippocampal neurons, clearance of large Ca 2+ loads was inefficient due to impaired mitochondrial Ca 2+ uptake. In contrast, neither Ca 2+ uptake by sarco/endoplasmic reticulum Ca 2+ ATPase, nor Ca 2+ extrusion through plasma membrane was affected by the Cln8 mutation. Excitotoxic glutamate challenge caused Ca 2+ deregulation more readily in Cln8 mnd than in wt neurons. We propose that neurodegeneration in human CLN8 disorders is primarily caused by reduced mitochondrial Ca 2+ buffering capacity. © 2011 Elsevier Ltd.

Mironova G.D.,Pushchino State University | Shigaeva M.I.,Russian Academy of Sciences | Gritsenko E.N.,Russian Academy of Sciences | Murzaeva S.V.,Russian Academy of Sciences | And 3 more authors.
Journal of Bioenergetics and Biomembranes | Year: 2010

The mechanism of tissue protection from ischemic damage by activation of the mitochondrial ATP-dependent K + channel (mitoK ATP) remains unexplored. In this work, we have measured, using various approaches, the ATP-dependent mitochondrial K + transport in rats that differed in their resistance to hypoxia. The transport was found to be faster in the hypoxia-resistant rats as compared to that in the hypoxia-sensitive animals. Adaptation of animals to the intermittent normobaric hypoxia increased the rate of transport. At the same time, the intramitochondrial concentration of K + in the hypoxia-sensitive rats was higher than that in the resistant and adapted animals. This indicates that adaptation to hypoxia stimulates not only the influx of potassium into mitochondria, but also K +/H + exchange. When mitoK ATP was blocked, the rate of the mitochondrial H 2O 2 production was found to be significantly higher in the hypoxia-resistant rats than that in the hypoxia-sensitive animals. The natural flavonoid-containing adaptogen Extralife, which has an evident antihypoxic effect, increased the rate of the mitochondrial ATP-dependent K + transport in vitro and increased the in vivo tolerance of hypoxia-sensitive rats to acute hypoxia 5-fold. The involvement of the mitochondrial K + transport in the mechanism of cell adaptation to hypoxia is discussed. © 2010 Springer Science+Business Media, LLC.

Goncharov N.V.,RAS Sechenov Institute of Evolutionary Physiology and Biochemistry | Avdonin P.V.,Russian Academy of Sciences | Nadeev A.D.,Russian Academy of Sciences | Zharkikh I.L.,Institute of General Pathology and Pathophysiology RAMS | Jenkins R.O.,De Montfort University
Current Pharmaceutical Design | Year: 2015

The volume of publications on the role of reactive oxygen species (ROS) in biological processes has been increasing exponentially over the last decades. ROS in large amounts clearly have detrimental effects on cell physiology, whereas low concentrations of ROS are permanently produced in cells and play a role as signaling molecules. An imbalance in ROS production and defense mechanisms can lead to pathological vascular remodeling, atherosclerosis being among them. The aim of this review is to examine different sources of ROS from the point of view of their participation in pathogenesis of atherosclerosis and related cardiovascular risk. Among the possible sources of ROS discussed here are mitochondria, NADPH-oxidases, xanthine oxidase, peroxidases, NO-synthases, cytochrome P450, cyclooxygenases, lipoxygenases, and hemoglobin of red blood cells. A great challenge for future research is to establish interrelations, feedback and feed-forward regulation mechanisms of various sources of ROS in development of atherosclerosis and other vascular pathologies. © 2015 Bentham Science Publishers.

Makarenko A.N.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

The processes of developed in CNS the complicated stroke and developments of fittings for their pharmaceutical therapy were developed and offering by standardized method of the experimental secondary stroke in rats, suitable for the use in sharp and chronic researches. Variant of repeated hemorrhagic stroke consist of autohemorrhagic right hemisphere stroke by the mechanical damage of brain tissue after 10-daily occlusion of right common carotid artery was studied. A model is comfortable for reproducing of the repeated standardized local damage of brain, is more adequate form of design of transient and chronic cerebrovascular pathology, than the independent use of local hemorrhage of autoblood in the brain of animals. The morphological description of model approaches the clinical variants of development and flow of sharp hemorrhagic stroke after a previous chronic cerebral insufficiency on an ischemic type.

Merkulov Y.A.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

Work with night shift is an obligate necessity of modem industrial urban society. In developed countries in the work on the night shift use up to 20%. These categories of workers are definitely the locomotive drivers. The consequence of a regular work with night shifts is a violation of human circadian rhythms, which, through dysregulation of the autonomic nervous system, is reflected in a greater risk of disease and transport accidents. The need to find ways and criteria of preventive monitoring dysregulatory changes in the human body is an urgent and challenging issue in terms of the health of the working population, disease prevention, and transportation security.

Nikoforov N.G.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

In the present review we focus on the major cellular and molecular processes leading to the formation and accumulation of foamy cells: increased transmigration of monocytes into sub-endothelial sites of inflammation, activation of macrophages, modifications of lipoproteins, different types of uptake of native and associated lipoproteins (endocytosis, phagocytosis, and less-investigated--patocytosis), as well as participation of different molecular systems in the reverse cholesterol transport in macrophages. Special attention is given to the recent data indicating that scavenger receptors participate not only in the uptake of modified lipoproteins, but also in the reverse cholesterol transport. In conclusion, we discuss most relevant open questions in our understanding of the mechanism and functional consequences of macrophage/lipoprotein interactions: which receptor systems are used for the recognition and internalisation of aggregated lipoproteins, what are the mechanisms of intracellular processing of associated lipoproteins, and how associated lipoproteins affect functional programming of macrophages.

Menzikov S.A.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

Effect of the glucose and Mg(2+)-ATP on the coupled with CABA(A)-receptor Cl-,HCO3(-)-activated Mg(2+)-ATPase of the plasma membranes from rat brain involving from "basal" Mg(2+)-ATPase which it is activated by Cl-,HCO3(-) ions it was investigated. The glucose (1-10 mM) decreased the "basal" Mg(2+)-ATPase activity on 17% and completely eliminated the enzyme activation by 10 mM Cl(-)+2 mM HCO3(-) ions. The variety effect of the glucose and Mg(2+)-ATP on the activation of the '"basal" Mg(2+)-ATPase by variety concentrations of anions it was established. So it was found that in the presence Mg(2+)-ATP in the incubation medium > 1 mM the enzyme activation by 10 mM Cl- + 2 mM HCO ions not appear. However, in the presence of the glucose (10 mM) the inhibiting effect of the Mg(2+)-ATP on the enzyme is disappears and Cl-,HCO3(-)-ATPase activity is restored. While, in the presence of the high concentrations 40 mM Cl- + 8 mM HCO3(-) in the incubation medium the inhibiting effect of the glucose and Mg(2+)-ATP it was negligible (-20%). It was conclusion about direct involvement of the glucose and Mg(2+)-ATP in the regulation of the coupled with CABA(A)-receptor Cl-,HCO3(-)-ATPase activity of the neuronal membrane under different concentration anions in the incubation medium.

Rebrov I.G.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

Functional activity of the CGABA(A)-receptor/Cl(-) ionophore complex was investigated the muscimol-stimulated entry of the radioactive isotope 36Cl(-) in synaptoneurosomes in changing the structure and permeability of neuronal membranes. Integrity of the membranes was damaged by removal of Ca(+2) and Mg(+2) from the incubation medium and by the method of freezing-thawing synaptoneurosomes. In both cases, an increase in basal 36Cl(-) entry into synaptoneurosomes, indicating increased nonspecific permeability of neuronal membranes, and decreased activity the CABA(A)-receptor/Cl(-) ionophore complex. The conclusion about the relationship of processes damage neuronal membranes and reducing the inhibitory processes in the epileptic focus.

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