National Repository of Grey Literature 40 records found  1 - 10nextend  jump to record: Search took 0.00 seconds. 
The role of AQP4 and TRVP4 channels in the ischemic brain edema: focusing on glial cells.
Kročianová, Daniela ; Anděrová, Miroslava (advisor) ; Máčiková, Lucie (referee)
Cerebral ischemia, also known as stroke, is one of the most common causes of death. It is accompanied by the formation of edema, which can be characterized as an influx of water and osmolytes into the brain, causing volume alterations. We recognize two types of cerebral edema - vasogenic, characterized by the disruption of the blood-brain barrier (BBB) and increase of the extracellular volume, and cytotoxic, caused by the increase of the volume of cells, mainly glia. The major contributors to the formation of cytotoxic edema are the astrocytes, which, in physiological conditions, are responsible for the maintenance of the BBB and keeping the homeostasis of the brain and spinal cord or central nervous system. The mechanism responsible for the process of volume and osmotic changes are the transmembrane channels, mainly aquaporin 4 (AQP4) and transient receptor potential vanilloid 4 (TRPV4). AQP4 is the main pathway for water influx as well as efflux when the edema subsides. TRPV4 is likely responsible for the maintenance of the osmotic balance of the organism, although its precise role in the formation of the edema has not yet been fully elucidated. The main aim of this thesis was to categorize the types of cerebral ischemia and edema, and to describe the process of cerebral edema formation and the...
The Role of Aquaporin 4 channels and Transient Receptor Potential Vanilloid 4 channels in astrocytic swelling
Heřmanová, Zuzana ; Anděrová, Miroslava (advisor) ; Machová Urdzíková, Lucia (referee)
Astrocytes posses a wide range of functions within the brain. In response to ischemic conditions they swell due to increased uptake of osmolytes and they are mainly responsible for cytotoxic edema formation. However, they are also able to regulate their volume by releasing osmolytes together with water via the process of regulatory volume decrease (RVD). The Aquaporin 4 (AQP4) channel and Transient receptor potential vanilloid 4 (TRPV4) channel are suspected to be strongly involved in these processes of astrocytic volume regulation. The goal of the present diploma thesis was to clarify the role of both channels in astrocytic swelling in situ. For our experiments we used a subpopulation of green fluorescent protein-labelled astrocytes from AQP4-deficient (AQP4-/- ), TRPV4-deficient (TRPV4-/- ) and control (Ctrl) mice. Cell volume alterations were induced in acute brain slices by hypoosmotic stress or by oxygen-glucose deprivation (OGD). Data were quantified using fluorescence intensity-based approach in the whole cells and in astrocytic endfeet. Our results indicate, that there is no difference in astrocytic swelling or cell volume recovery between astrocytes from AQP4-/- , TRPV4-/- and control mice when exposed to hypoosmotic stress. On the contrary, volume changes induced by OGD varied...
Steroid - NMDA receptor interaction: Structure-activity study and effect on mutant forms of human NMDA receptors
Krausová, Barbora ; Vyklický, Ladislav (advisor) ; Anděrová, Miroslava (referee) ; Tureček, Rostislav (referee)
N-methyl-D-aspartate (NMDA) receptors are glutamate-gated calcium permeable ion channels that play a key role in excitatory synaptic transmission and plasticity, and their dysfunction underlies several neuropsychiatric disorders. The overactivation of NMDA receptors by tonically increased ambient glutamate can lead to excitotoxicity, associated with various acute and chronic neurological disorders, such as ischemia, Alzheimer and Parkinson's disease, epilepsy or depression. On the opposite, NMDA receptor hypofunction is thought to be implicated in autism, schizophrenia, or intellectual disability. Recent DNA screening for neurological and psychiatric patients revealed numerous mutations in genes encoding for NMDA receptor subunits. The activity of NMDA receptors is influenced by a wide variety of allosteric modulators, including neurosteroids that could both inhibit and potentiate the activity of NMDA receptors, which makes them promising therapeutic targets. In this thesis, we describe new classes of neurosteroid analogues which possess structural modifications at carbons C3 and C17 of the steroidal core, and analogues without D-ring region (perhydrophenanthrenes). We evaluated the structure-activity relationship (SAR) for their modulatory effect on recombinant GluN1/GluN2B receptors. Our results...
DISP3/PTCHD2 function in neural cells
Konířová, Jana ; Bartůněk, Petr (advisor) ; Anděrová, Miroslava (referee) ; Pacherník, Jiří (referee)
DISP3 protein, also known as PTCHD2, belongs to the PTCHD family of proteins, which contain a sterol-sensing domain in their structure. The expression of the Disp3 gene is high in neural tissues and is regulated by thyroid hormone. The DISP3 gene is associated with development and progression of certain types of tumors, as well as with development of some neural pathologies. Neural stem cells also display high expression of the Disp3 gene. Neural stem cells are defined by their capability to self-renewal and capacity to differentiate into the basic types of neural cells - neurons, astrocytes, and oligodendrocytes. Precise regulation of the balance between proliferation and differentiation of neural stem cells is crucial for development of the central nervous system and its subsequent proper functioning, and disruption of this balance may lead to development of various pathologies. In this work we mainly focused on describing the function of the DISP3 protein in neural cells and tissues. We have shown that during differentiation of neural stem cells, the expression of the Disp3 gene is significant decreased. Furthermore, we have found that in neural stem and progenitor cells, the increased expression of the Disp3 gene promotes their proliferation. Moreover, when Disp3 expression was disrupted, the...
Glial cells and their role in amyotrophic lateral sclerosis
Vaňátko, Ondřej ; Anděrová, Miroslava (advisor) ; Černý, Jan (referee)
Amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease) is a progressive neurodegenerative disorder. It affects upper and lower motor neurons in the brain motor cortex, the brain stem and the spinal cord, causing their death, which results in denervation of voluntary muscles. Progressive muscle weakness and atrophy throughout the entire body gradually leads to worsening of the ability to move, speak, chew, swallow and eventually breath. Ultimately it results in affected individual's death due to respiratory muscle failure. Although first identified in 1869, no cure for ALS has been yet found. While early studies focused mainly on the research of motor neurons themselves, the attention has shifted towards glial cells in the past two decades. Glial cells are essential for proper neuron functioning and survival and it appears that they play a major role in ALS progression. The goal of this thesis is to review and summarize findings on the role of glial cells in ALS over the last years, focusing on four specific types of glial cells, namely astrocytes, microglia, oligodendrocytes and NG2-glia. Key words: amyotrophic lateral sclerosis, ALS, motor neuron, glia, astrocyte, microglia, oligodendrocyte, NG2-glia
The effect of the canonical Wnt singalling pathway on the differentiation of polydendrocytes after ischemic brain injury
Knotek, Tomáš ; Anděrová, Miroslava (advisor) ; Romanyuk, Natalyia (referee)
Polydendrocytes, or NG2 glia, are fourth type of glial cells in mammal central nervous system. In the adult brain, NG2 glia represent important cell type with respect to their role in gliogenesis and nervous tissue regeneration following injury. Ligands from the Wingless/Int (Wnt) family play key role in proliferation and differentiation of NG2 glia and they can also influence regeneration of nervous tissue after ischemia. The aim of this thesis was to elucidate the role of NG2 glia in neurogenesis and gliogenesis following ischemic brain injury and investigate the impact of Wnt signalling on the reaction of NG2 glia to this type of injury. To fulfil these aims, transgenic mouse strains with tamoxifen-inducible recombination, that enabled simultaneous expression of red fluorescent dye and either activation or inhibition of the Wnt signalling pathway in NG2 glia, were employed. To induce ischemic injury, middle cerebral artery occlusion model was used. Changes in differentiation and electrophysiological properties of NG2 glia were analysed using patch-clamp technique. Activation of the Wnt signalling pathway under physiological conditions and 7 days after ischemic injury led to increased differentiation of NG2 glia toward astrocytes, while 3 days after ischemic injury activation of this signalling...
Proteomic analysis of cellular proliferation and differenziation: Model of neural stem cells and cancer cells
Skalníková, Helena ; Kovářová, Hana (advisor) ; Anděrová, Miroslava (referee) ; Bezouška, Karel (referee)
CoNcLUsIoNs In protein profiling of neural stem cells using 2-dimensional gel electrophoresis and mass spectrometry, constitutively expressed proteins in 66 protein spots were identified. Most of the individual protein species were related to RNA and protein metabolism, processing and turnover, including some chaperones and stress response proteins. Proteins involved in cellular organization (e.g. cýoskeletal proteins and annexins), metabolic proteins (mostly enrymes),cellular energetics,cell defenseand signallingfollowed in lower numbers. Proteins in 16 spots significantly regulated during neural differentiation were identified. Induction of levels of o-B crystallin, hnRNP Al and hnRNP AZIBI during differentiation and protein localization within neural cells were studied by westernblottingand immunocýochemistry. Using antibody microarrays, in neural stem cells an increase in GRK2 level and phosphorylationsof signalling molecules(CDKI|Z, PKC mu, PKCy, Erk5 and o-B crystallin) involved mostly in cellular proliferation were detected.On the contrary, in differentiatedneural cells levels of protein-phosphatase4, heme-oxygenase2, MEK3, RafB, pro-caspase 1 and phosphorylation of 40 kDa proline-rich Akt substratewere induced. In cancer cells after protein separationby ProteomelabrM PF 2D system, 8 proteins...
The role of astrocytes in the formation of brain edema
Heřmanová, Zuzana ; Anděrová, Miroslava (advisor) ; Pačesová, Dominika (referee)
Brain edema is a cause of mortality accompanying number of pathologies such as ischemia, traumatic brain injury, tumors or liver and kidney failure. It is described as a process of osmotic and water flux alterations, which lead to cell volume changes and to an increase in intracranial pressure. Brain edema is usually classified into two types: vasogenic and cytotoxic. Development of vasogenic edema is connected to the blood brain barrier disruption. Water accumulates in the extracellular space and exerts pressure on the cellular compartments of the tissue. The cytotoxic type of edema is characterized by water accumulation within the cells. The process of cellular volume enlargement is termed cellular swelling. Cytotoxic swelling is usually connected to glial cells, namely astrocytes, as these cells represent a part of the blood brain barrier and thus they influence homeostasis inside the brain. Water flows across cytoplasmic membrane through a system of specialized channels - aquaporins. For the brain edema formation, aquaporin 4 is the most important. It is localized on astrocytic membranes and using aquaporin-null mice, it has been shown, that it participates in water clearance in physiological and pathological conditions. Since the water fluxes are passive, the driving force for edema formation...

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