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1
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Protein serine/threonine kinases (PKA, PKC and CaMKII) involved in ischemic brain pathology

100%
Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
579-585
EN
The protein serina/threonine kinases which are highly expressed in the central nervous system (CNS) are severely affected by brain ischemia.Irrespective of substantial differences among the particular members of this group of kinases, their responses to ischemic stress show a lot of similarities.Initially they are switched on fy faciliated interaction with their specific activators/second messengers like cyclic AMP, 1,2 -sn-diacylglicrol and particularly Ca2+, then they are translocated to highly specific regions of plasma membranes.After phosphorylation of target proteins, the kinases are deactivated by means access to cAMP. In the case of CaMKII, it is probably achieved by its extensive, inhibitory autophosphorylations, while PKC seems to be proteolytically degraded.These biphasic changes in serine/threonine kinases activity may play a critical role in the evolution of postichemic brain injury and provide a mechanism for a variety of short- and long-term signalling events.
2
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Enhancement of [3H]D-aspartate release during ischemia like conditions in rat hippocampal slices:source of excitatory amino acids

64%
Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
63-70
EN
Ischemic neuronal injury is supposed to be caused in part by the extracellular accumulation of excitatory amino acids (EAA). Neurotransmitter and metabolic EAA can be released from synaptic vesicles and cytoplasm of neurones and glial cells. In this study the release of the glutamate analogue [3H]D-aspartate (3[H]D-ASP), loaded into 500 mugm slices of rat hippocampus, was investigated. The efflux of the label was measured during anoxic - aglycemic ("ischemic") and normoxic K+ depolarization. To identify the pools from which [3H]D-ASP is released we have estimated its calcium dependence and the effects of inhibitors of: (1) Na+ - dependent transporter of amino acids (100 mugM L-trans-pyrrolidine-2,4-dicarboxylic acid /L-trans-PDC/), (2) sodium channel (1 mugM tetrodotoxin TTX), and (3) anion channel (1mM furosemide). [3H]D-ASP released upon normoxic depolarization was 40% inhibited by TTX,nearly 40% by L-trans-PDC and over 50% by furosemide. The "ischemic" release was in 40% calcium dependent, completely TTX independent and in approximately 50% blocked by furosemide treatment. Our data suggest that EAA accumulated in the synaptic cleft during ischemia are mainly released from the cytosolic compartment by mechanisms wich are connected with the ischemic increase of extracellular potassium concentration.
3
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Rabbit paralytic tremor phenotype- A plp1 gene mutation as a model of human Pelizaeus-Merzbacher disease

64%
Sypecka J., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
221-230
EN
The paralytic tremor (pt) disease in rabbits results from a point mutation in a plp gene and manifests itself by a broad range of neurological signs. Biochemical studies have shown that myelinogenesis is retarded and deficient in mutant rabbits. Myelin sheaths are usually thin and malformed. The number of oligodendrocytes is normal, however their differentiation and maturation is prolonged. The effects of the pt mutation were investigated in morphological, biochemical and molecular studies, resulting in the well-documented characteristics of the disease. The pt phenotype and its detailed characteristics make the mutated rabbit a good model of Pelizaeus-Merzbacher disease.
4
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Involvement of MMPs in delayed neuronal death after global ischemia

51%
Zalewska T., Ziemka-Nalecz M., Sarnowska A., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2002
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vol. 62
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issue 2
53-61
EN
Spatial and temporal relations between metalloproteinase (MMP-2 and MMP-9) activation and laminin degradation in gerbil hippocampus after transient cerebral ischemia has been studied. Activity of MMPs was determined by gelatin zymography in homogenates from dorsal (DP, an equivalent of CA1 sector) and abdominal (AbP, containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of both investigated metalloproteinases was found at 72 h of recovery. Whereas MMP-2 up-regulation did not show any spatial preferences, the increase of MMP-9 activity was observed exclusively in DP. Activation of MMP-9 at this time point correlated spatially with degradation of laminin - protein of extracellular matrix. These results show that MMP pathway may function as a component of delayed neuronal death cascade in the apoptogenic CA1 sector after transient global ischemia.t
5
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Laminin promotes oligogliogenesis and increases MMPs activity in human neural stem cells of HUCB-NSC line

51%
Sypecka J., Dragun-Szymczak P., Zalewska T., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
37-45
EN
Oligodendrocytes, the cells responsible for myelin formation and maintenance in CNS, are depleted in many acute and chronic conditions. The stem/progenitor cells stimulation or transplantation might be seriously considered as a long hoped for therapeutic perspective. Better understanding of the mechanism(s) regulating the activation of the cell lineage from the endogenous progenitor reservoir might be helpful. Therefore an efficient source of donor cells for transplantation in humans is being craved for. In this study we show that the application of extracellular matrix component-laminin promotes oligogliogenesis from neural stem-like cells of human cord blood cells (HUCB-NSC). Although oligodendrocytes constitute a minor subpopulation of spontaneously differentiated HUCB-NSC, the manipulation of active compounds regulating the process of cell commitment results in a several fold increase in their number. Thus cells of the HUCB-NSC line could be considered as a potential source of glial cells, fulfilling the suitable candidate criteria for oligodendrocyte replacement therapy.
6
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Housing conditions influence motor functions and exploratory behavior following focal damage of the rat brain

51%
Gornicka-Pawlak E., Jablonska A., Chylinski A., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
62-72
EN
The present study investigated influence of housing conditions on motor functions recovery and exploratory behavior following ouabain focal brain lesion in the rat. During 30 days post-surgery period rats were housed individually in standard cages (IS) or in groups in enriched environment (EE) and behaviorally tested. The EE lesioned rats showed enhanced recovery from motor impairments in walking beam task, comparing with IS animals. Contrarily, in the open field IS rats (both lesioned and control) traveled a longer distance, showed less habituation and spent less time resting at the home base than the EE animals. Unlike the EE lesioned animals, the lesioned IS rats, presented a tendency to hyperactivity in postinjury period. Turning tendency was significantly affected by unilateral brain lesion only in the EE rats. We can conclude that housing conditions distinctly affected the rat.s behavior in classical laboratory tests.
7
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Changes of Ca2+/calmodulin - dependent protein kinase-II after transient ischemia in gerbil hippocampus

51%
Zalewska T., Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
41-48
EN
Transient cerebral ischemia induces, besides delayed neurodegeneration in selected brain structures, a number of early responses which may mediate ischemic injury/repair processes. Here we report that 5 min exposure to cerebral ischemia in gerbils induces a rapid inhibition and subsequent translocation of Ca (2+)/calmodulin-dependent protein kinase II (CaMKII). These changes were partially reversible during a 24 h post-ischemic recovery. Concomitantly the total amount of the enzyme protein, as revealed by Western blotting (alfa- -subunit specific), remained stable. This is consistent with our previous hypothesis, that the mechanism of ischemic CaMKII down-regulation involves a reversible posttranslational modification-(auto)phosphorylation, rather then the degradation of enzyme protein. The effectiveness of known modulators of postischemic outcome in counteracting CaMKII inhibition was tested. Three of these drugs, namely dizocilpine (MK-801), N-nitro-L-arginine methyl ester (L-NAME) and gingkolide (BN52021), all significantly attenuated the enzyme response to ischemia, whereas an obvious diversity in the time-course of their actions implicates different mechanisms involved.
8
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Phosphorylation of Protein Kinase C substrate proteins in rat hippocampal slices - effect of calpain inhibition

51%
Domanska-Janik K., Zablocka B., Zalewska T., Zajac H.
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vol. 58
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issue 4
247-252
EN
Incubation of the acutely dissected rat hippocampal slices in calcium-containing media resulted in spontaneous activation-translocation of classical PKC isoforms and their subsequent (especially g- type) proteolytic degradation. These changes were blocked by calpain inhibitor MDL 28 170 in 100 mM concentration. Rat hippocampal slices were metabolically prelabelled with 32Pi and stimulated with NMDA/glycine, depolarization or phorbol dibutyrate (PDBu) treatment. The basal phosphorylation of specific PKC substrates (MARCKS, neuromodulin and neurogranin) was significantly reduced in non-stimulated slices by MDL pretreatment. In contrast, only the slices where calpain activity was inhibited responded to further NMDA or phorbol dibutyrate stimulation by a substantial increase of PKC-dependent protein phosphorylation. It is concluded that the PKC phosphorylation system is severely affected by non-specific activation and a subsequent, calpain-dependent proteolysis in the acutely prepared hippocampal slices. Calpain inhibition by 100 mM MDL partially prevented these changes and increased stimulus-dependent phosphorylation of PKC-specific protein substrates.
9
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Neural commitment of cord blood stem cells (HUCB-NSC/NP): Therapeutic perspectives

51%
Domanska-Janik K., Habich A., Sarnowska A., Janowski M.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
279-291
EN
Human umbilical cord blood (HUCB) is considered a promising source of neural progenitors capable of being used for cellular therapies in neurological disorders. Here we review briefly our work on the elucidation of mechanisms and development of practical standards as regards the selection, maintenance and use of cord blood derivatives for such purposes. Our results join those of other recent studies in suggesting strongly that, the generation of neural-like cells from tissue belonging to a different germ layer (such as a cord blood is) is most probably explained by reference to a discrete subpopulation of embryonic-like stem cells of pluripotent characteristics. Such cells identified in cord blood through their expression of specific genetic and protein markers can be expanded in vitro and directed toward neurally-committed progenitors differentiating further into more mature neuron-like or macroglia-like cell phenotypes. From this HUCB-derived neural progenitor fraction a novel neural-like stem cell line (HUCB-NSC) has been developed, and characterized in respect of in vitro and in vivo (post-transplantation) properties.
10
Content available remote

Interrelations between nuclear-factor kappa B activation, glial response and neuronal apoptosis in gerbil hippocampus after ischemia

51%
Domanska-Janik K., Bronisz-Kowalczyk A., Zajac H., Zablocka B.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 1
45-51
EN
Spatial and temporal relations between transcriptional factor NFkB activation and glia reaction in gerbil hippocampus after transient cerebral ischemia has been studied. Activation of protein binding to NFkB consensus oligonucleotide was determined by electrophoretic mobility gel shift assay (EMSA) in homogenates from dorsal (DP- an equivalent of CA1 sector) and abdominal (AbP- containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of NFkB binding was observed exclusively in DP as early as 3 h after ischemia and at this time that response preceded any other morphological signs of postischemic tissue injury. This early enhancement of NFkB binding was followed by microglia activation visualized in CA1 pyramidal region at 24 h of recovery by histochemical staining with lectin from Ricinus communis (RCA-120). Simultaneously, only a moderate increase of immunostaining against glial fibrillary acidic protein (GFAP) was observed homogeneously in all parts of hippocampus. This uniform pattern of astrogliosis was preserved until postischemic day 3-4, when apoptotic DNA fragmentation in CA1 pyramidal neurons had been clearly documented by TUNEL staining. At this period however, continuous elevation of NFkB binding in DP corresponded with similar response manifested also in AbP of the hippocampus. These results evidence a preferential NFkB involvement in an early microglia activation in the apoptogenic CA1 sector, although its role in a later astrocytic response to ischemia could not be neglected too.
11
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Patterned growth and differentiation of human cord blood- derived neural stem cells on bio-functionalized surfaces

33%
Buzanska L., Ruiz A., Zychowicz M., Rauscher H., Ceriotti L., Rossi F., Colpo P., Domanska-Janik K., Coecke S.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
24-36
EN
Bio-functionalized surfaces were prepared to study the adherence and differentiation capacity of neural stem cells derived from human umbilical cord blood (HUCB-NSC). Cell growth platforms containing arranged arrays of adhesive molecules were created by microcontact printing on a biologically inert surface. Biomolecules used to prepare microarray platforms included the extracellular matrix protein fibronectin and the polyaminoacid poly-L-lysine. HUCB-NSC plated on microplatforms at various serum conditions showed serum and molecule type dependent capacity for adhesion and differentiation. Poly-L-lysine allowed the maintenance of stem-like non differentiated cells attached to the surface, whereas fibronectin promoted spreading and neural commitment. Serum deprivation did not influence the attachment of HUCB-NSC to fibronectin, but significantly enhanced the attachment to poly-L-lysine and promoted dBcAMP induced neuronal differentiation. A bio-pattern of squares with interconnecting lines was used to guide neuronal differentiation by directing cell protrusion outgrowth. Tailoring the geometry of the bio-pattern enabled directing and monitoring of the neural stem cells. development in the large scale multiparameter biotests.
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