Wyniki wyszukiwania

1

Apoptoza i metody jej identyfikacji.

100%

Sulejczak D.

Postępy Biologii Komórki

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2000

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tom 27

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nr 4

527-568

2

Temporal changes in Bel-2 and Bax proteins in rat cerebral cortex following devascularizing lesion

63%

Sulejczak D., Skup M.

Acta Neurobiologiae Experimentalis

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2001

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tom 61

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nr 3

3

Axoplasmic localisation of the NFkappaB p65 subunit in the rat brain

63%

Sulejczak D., Skup M.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 2

4

Selected biochemical characteristics of the rat mhSOD1(G93A) transgenic model of familial amyotrophic lateral sclerosis (fALS) and the effects of cytidine 5-diphosphocholine (sodium salt, CDPch) treatment

51%

Chrapusta S. J., Herbik M. A., Sulejczak D., Grieb P.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Background: Massive expression in rats of the mutated human superoxide dismutase-1 gene (mhSOD1G93A) causes an incurable, fast-progressing fatal illness that is an established model of fALS. We showed earlier that CDPch can slightly but signifi cantly defer the onset of neurologic symptoms and extend life of the carriers. Here we report effects of the drug on some biochemical indices. Methods: Transgenic mhSOD1G93A(+) (Tg+) rats were randomized by gender and litter between study groups. The treatments began on postnatal day (PD) 61, consisted of a daily ip dose of CDPch (0.5 g/kg) or isotonic NaCl, and continued for a preset time or until an arbitrary (the rats were euthanized when unable to feed voluntarily) death point. Untreated Tg+ rats (PD 50ñ60, 94 and 108ñ129) and their Tg-siblings were used for additional controls. After decapitation, blood serum and CNS were harvested and stored at −80°C till analyzed. Results: ANOVA showed signifi cant (P<0.001) age-related elevation of serum immunoreactive mhSOD1 (s-ir-mhSOD1) in NaCl-treated Tg+ rats, signifi cantly (P=0.011) higher s-ir-mhSOD1 level in NaCl-treated terminal stage Tg+ rats than in their CDPch-treated counterparts, and a signifi cant interaction (P=0.02) between these factorsí effects on s-ir-mhSOD1 level; no such effect was found in serum VEGF or spinal cord ir-mhSOD1 level. There was signifi cant (P<0.01) lowering effect of CDPch treatment, a tendency (P=0.09) for agerelated lowering and a tendency (P=0.10) for interaction between these factorsí effects on serum total thiol (sTT) level; post-hoc analysis showed signifi cantly lower sTT level in CDPch-treated terminal stage rats than in their NaCl-treated counterparts. Western blots showed the existence of multiple oligomeric forms of s-ir-mhSOD1 in Tg+ rats.

5

Expression of purinergic P2X(7) receptor in rat brain during the symptomatic phase of experimental autoimmune encephalomyelitis and after recovery of neurological deficits

51%

Grygorowicz T., Sulejczak D., Struzynska L.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr 1

Purinergic ionotropic P2X7 receptor is widely distributed in brain. Strong evidence suggests that this receptor is related to inflammatory and neurodegenerative changes in many pathological states of central nervous system (CNS), including multiple sclerosis (MS). Experimental autoimmune encephalomyelitis (EAE) is the commonly used animal model of MS. In this study we investigate the expression of P2X7R protein in rat brain in the symptomatic phase of EAE (day 10 post immunization) and after reversion of neurological symptoms (day 20 p.i.). We found the increased level of P2X7R protein in brain homogenates of EAE rats in both examined time windows. Immunohistochemical study revealed enhanced receptor's immunoreactivity. Immunoblots done with isolated cellular brain fractions indicated that the P2X7R overexpression is related to synaptosomal fraction in the symptomatic phase and to the glial (GPV) fraction in the recovery phase of EAE. Concomitantly, we noticed overexpression of astroglial marker GFAP in brain homogenates and astroglial fraction (GPV), so as its enhanced immunoreactivity in brain sections (10 days p.i.) which did not decline to control values in the recovery phase, similarly to P2X7R expression. Results suggest the involvement of P2X7R-mediated signaling in the pathomechanisms of EAE with the possible relevance of astrocytic pool of cells.

6

Phenotypes of cell pools populating the injury site in a rat model of surgical brain cortex lesion

51%

Frontczak-Baniewicz M., Chrapusta S. J., Sulejczak D.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Because of their potential for self-renewal and the ability for generating many differentiated cell types, progenitor cells are a key player in regenerative and repair processes. In the central nervous system, pools of these cells have been identified in two regions: the subgranular zone of hippocampal gyrus dentatus and the subventricular zone. Neural stem cells that reside in these regions are subject to a specific neurogenesis-stimulating and -regulating environment called ‘niche’. Our model of surgical brain injury (SBI) opens the avenues for studying the mechanisms of repair and reconstruction of brain cortex and enables demonstrating the presence of possible vascular niches in the peri-lesion zone. The present studies were aimed at characterizing of the immune phenotype of the cells that populate this region. The peri-lesion area of the brain cortex showed the presence of dying neurons and glial cells since the first postlesion day. Simultaneously, activated microglial cells and astrocytes appeared, and part of the latter formed a scar on the surface of the damaged cortex. Another fractions of the cells that appeared following the SBI in both the lumen and the vicinity of blood vessels expressed either the macrophagal/monocytic marker CD14, or the marker of hematopoietic progenitor cells and small vessel endothelium CD34. Beginning on the first post-SBI day, the peri-lesion area showed also the presence and accumulation of a variety of cells with immature phenotypes. These included immature endothelial cells building new blood vessels (angiogenesis) and cells with phenotypes of other brain parenchyma-forming cell subpopulations: (1) nestin-positive astroglial and non-glial cells, (2) cells expressing the marker of juvenile astrocytes vimentin-positive, and (3) cells showing doublecortin immunoreactivity (the marker of early differentiated neurons). These results clearly indicate that during the early post-SBI period the peri-lesion zone is being populated by a heterogenic pool of morphologically immature cells that most likely herald the advent of reconstruction and/or repair of the injured brain region. Supported by the Polish Ministry of Science and Higher Education grant No N N404 522838

7

Diversity of immunophenotypes of endothelial cells participating in new vessel formation following surgical rat brain injury

51%

Frontczak-Baniewicz M., Walski M., Sulejczak D.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 5

8

Endothelial progenitor cell in newly-formed capillaries following surgical brain injury of rat cerebral cortex

51%

Frontcak-Baniewicz M., Walski M., Sulejczak D.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Several lines of evidence suggests that neovascularization in adult organism may be mediated by circulating progenitor cells. During ischemia and brain injury, populations of endothelial progenitor cells are mobilized and recruited to ischemic and injured areas, accelerating the neovascularization process. Surgical brain injury causes neovascularization in the disrupted brain parenchyma, which occurs with participation of endothelial-like cells. The aim of study was comparison of ultrastructural and immunohistochemical features of endothelial progenitor cells participated in new vessel formation following surgical brain injury in non-diabetic and diabetic rats. We investigated subcellular localization of protein markers: Flk-1, AC133 and vimentin. We detected the presence of immature endothelial cells showing positive immunostaining for all investigated markers in the proximity to the injured brain area in diabetic rats. Only few these cells were observed in the brains of non-diabetic animals. Ultrastructural studies showed many morphological changes within capillaries in the injured brain derived from diabetic animals. Our results point to the diabetes related dysfunction of the brain capillaries. The number of progenitors and, probably, their abnormal differentiation contribute to disorders in the process of repair following the injury in diabetes-affected rats.

9

Zwierzęcy model lipopolisacharydowego zapalenia płuc

51%

Welniak-Kaminska M., Kopczynska B., Sulejczak D., Grieb P.

Prace i Materiały Zootechniczne

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2008

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tom 66

10

Neurovascular unit and glial scar formation following the surgical brain injury

51%

Frontczak-Baniewicz M., Sulejczak D., Czajkowska D., Grieb P.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr 1

Normal functioning of both the CNS and the blood-brain barrier depends on proper functioning of the neurovascular unit (NVU) - a dynamic structure made of neurons, capillary vessel (consisted of endothelial cells, pericytes and basement mebrane), extracellular matrix and vessel-bound astrocytes. Human brain trauma occurs during numerous life-saving neurosurgical procedures (e.g. removal of a brain tumor) associated with disrupted continuity of the meninges followed by interventions within the cerebral parenchyma. Such interventions result in damage to all morphological components of NVU. Our rat model of cerebral cortex injury imitates quite well the respective human neurosurgery situation in that it involves the most typical early and delayed consequences of neurosurgical procedures. This model, enables studying the cortical response to the lesion at cellular and subcellular levels and relating them to the underlying biochemical changes. The injury is being made by excising of a moderate-sized (about 2.5 mm × 2.5 mm × 1.5 mm, length × width × thickness) piece of sensorimotor cortex in the frontotemporal region and resulting in the massive damage of that area. Within first few hours following the lesion the border zone of the damage area showed a perivascular astrocytic edema. Two days after the injury, a massive angiogenesis was observe in this region. Formation of new blood vessels occurred even 30 days after the lesion. Beginning on postinjury day 4, the area around the wound showed an increase in both the number and hypertrophy of astrocytes, that showed an enhance of immunoreactivity for the main astrocytic markers: vimentin and GFAP. Fifth postlesion week a well-formed scar was observed within the operated area. However, 3 months after the operation astrocytic processes began to show an edema, and shortly thereafter the scar presented signs of lysis and dissolution. Beginning 24 hours after the injury, the cortex adjacent to the injury showed the presence of degenerating necrotic and, particularly at later time points, of apoptotic neurons. Our studies reveal that the damage and remodeling of the surgical brain injury zone and its vicinity, as well as forming of the glial scar do not mark an end of the process initiated by the cortical injury. Despite completion of these processes, the area adjacent to the damage was always subject to a secondary damage resulting in brain parenchyma loss that reached far beyond the primary injury zone. Supported by ministry of Scientific research and Information Technology. Project nr N404522838

11

Surgical injury-induced early neocortical microvascular changes and characteristics of the cells populating the peri-lesion zone

51%

Sulejczak D., Chrapusta S. J., Kozlowski W., Frontczak-Baniewicz M.

Acta Neurobiologiae Experimentalis

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2016

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tom 76

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nr 2

Adult mammalian brain contains a number of specialized neurovascular structures termed “niches” that act as sources of neuronal cells throughout the individual’s life. Some of the niches generate neurons to satisfy the need for ‘replacement’ neurons within the same or closely located brain structures, whereas the other can provide such cells for more distant destinations in the brain. A common characteristic of known neurovascular niches is the presence of a complex 3-dimensional network of basal lamina processes, called fractones. It apparently plays a major role in communication between the various niche-populating cell types as well as in niche activity and output. We hypothesized that similar niches may form ad hoc after a mechanical brain trauma, and tested this possibility in a rat model of surgical brain injury. Four days after removing a small fragment of sensorimotor cortex, the peri-wound region showed numerous symptoms of active repair and remodeling of brain parenchyma, including the presence of multiple cell types of immature phenotypes. The latter, as shown by a variety of light and electron microscopy techniques, included endothelial cell precursors as well as nestin-positive immature neural cells of astrocytic or non-glial characteristics. However, there was no evidence of in situ neurogenesis or a considerable migration of cells from SVZ. The centers of the said repair processes were capillary blood vessels connected with basal lamina-formed fractones. These results indicate that surgical brain trauma causes the formation of a vascular niche with no apparent neurogenic potential.

12

Glial expression of purinergic P2X7 receptor in rat brain during the course of experimental autoimmune encephalomyelitis

51%

Grygorowicz T., Sulejczak D., Sulkowski G., Struzynska L.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr 1

Multiple sclerosis is a common neurodegenerative disease with prevalence in Poland about 15 per 10000 people. It is characterized by inflamed lesions in myelin sheaths surrounding axons in the white matter of the brain and spinal cord. These changes lead to the damage of axons and, in consequence, to a broad spectrum of neurological symptoms. Experimental autoimmune encephalomyelitis (EAE) is the well known and commonly used animal model of MS. In the present study the temporal pattern of glial activation (microglia and astroglia) together with P2X7R expression were investigated in brain of Lewis rats during the course of EAE. This receptor, activated under pathological conditions, may participate in the regulation of inflammatory response and cell death. It was shown to induce the release of inflammatory mediators like Il-1b and TNF-a in different types of glial cells. It is also pathologically involved in the release of potentially cytotoxic substances like glutamate and ATP. Western blot analysis was used to assess the relative concentration of P2X7R protein in glial fraction whereas its cellular localization was studied by immunohistochemical method. Tissue was labeled with the specific markers (Iba1 - microglial marker, GFAP - astroglial marker) and examined in the different stages post immunization (2, 4, 6, 8, 10 days). We observed the early overexpression of P2X7R protein (2-4 d.p.i.) in glial fraction obtained from brains of EAE rats with parallel enhancement of glial markers. Double immunofluorescent labeling showed colocalization of the receptor with glial markers. The results revealed that activation of both astroglia and microglia takes place very early post immunization, well before the neurological symptoms of the disease occur and is temporary connected with the overexpression of P2X7R. This suggests the involvement of P2X7R-mediated signals into the early pathological mechanisms operating during the disease.

13

Dootrzewnowe podanie 2-deoksyglukozy - szczurzy model glukodeprywacji mózgowej

51%

Sulejczak D., Welniak-Kaminska M., Bilmin K., Grieb P.

Prace i Materiały Zootechniczne

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2008

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tom 66

14

Unilateral photothrombotic stroke in the frontal cerebral cortex causes biiateral impairment of skilled movements of the rat forelimb

45%

Sulejczak D., Skup M., Stzralkowski R., Macias M., Czarkowska-Bauch J.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

15

Astroglial reaction in the early asymptomatic phase of experimental autoimmune encephalomyelitis

45%

Grygorowicz T., Sulkowski G., Sulejczak D., Lenkiewicz A., Struzynska L.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Under different pathological conditions activation of astrocytes of neuroprotective or neurotoxic nature is observed. There is a growing number of evidence that many pathological states of brain are characterized by very early active contribution of astrocytes to neurodegenerative axonal damage. Astroglia posses defense mechanisms against glutamate excitotoxicity (transporter systems) but may also contribute to the enhanced release of this potentially toxic amino acid trough exocytosis, P2X7 purinergic receptors, hemichannels or reversing of glutamate transporters. These cells are also a main source of ATP, active signaling molecule, which activates many purinergic receptors in brain, including P2X7R, which participates in development of infl ammation and neurodegeneration phenomena. The aim of this study was to investigate the expression of astroglia-specifi c proteins during the course of EAE using immunochemical and immunohistochemical analysis. We observed early activation of astroglia in the inductive phase of EAE (4 day p.i.) which was connected with overexpression of GFAP and S-100β. Expression of Cx43, protein that forms hemichannels was also enhanced so as the expression of P2X7R. Additionally, the level of GLT-1 glutamate transporter’s protein increase signifi cantly. The results suggest that in EAE pathology very early activation of astroglia takes place in the preclinical stage of the disease. The exact nature of this activation will be investigated.

16

Distribution of TrkB receptors in motor-sensory cortical areas in the rat

45%

Macias M., Dwornik A., Sulejczak D., Czarkowska-Bauch J., Skup M.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 3

17

Immunoexpression of the selected compounds of the SMN complex in spinal cord neurons in patients with sporadic amyotrophic lateral sclerosis (sALS)

45%

Dziewulska D., Sulejczak D., Chrzanowska H., Ogonowska W., Rafalowska J.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease leading to degeneration and loss of motoneurons in the spinal cord anterior horns. Although etiology of the disease is unknown there is a hypothesis assuming that survival motor neuron protein (SMN) may save motoneurons from degeneration not only in spinal muscular atrophy (SMA) but also in ALS. In animal models of ALS the neuroprotective role of SMN was observed but it is not known whether the phenomenon is present in humans. Therefore we decided to examine immunoexpression of SMN and functionally associated with it gemin 2, 3 and 4 in the anterior horn neurons of patients with sporadic form of ALS (sALS). Material and methods: The material was composed of 10 spinal cords of patients with sALS who died at the age of 52–87 years 1–8 years after the onset of the disease. On formalin-fixed and paraffin-embedded spinal cords immunohistochemistry was applied. The immunohistochemical reactions were performed with antibodies against SMN and gemin 2, 3 and 4 according to the avidin-biotin-peroxidase method. Results: In all the examined cases expression of SMN and gemin 3 in spinal cord neurons was found although intensity of the immune reactions was diverse. The immunolabel were the most intense in patients with acute course of sALS and gradually decreased with longevity of the disease. Not only motoneurons but also interneurons and sensory neurons revealed immunoexpression of SMN and gemin 3. The immune reaction to gemin 2 was negative. The immunoreactivity for gemin 4 was also negative or very weak. Conclusions: (1) In humans, expression of SMN and gemin 3 in neurons is present through the whole lifespan. (2) In sALS, expression of gemin 2 and 4 is abnormal: absent or diminished respectively. (3) Presence of all components of the SMN-gemin complex is probably necessary for its normal functioning. (4) Since the immunoreactivity for SMN, and gemin 2, 3 and 4 was similar in all the examined cases and 6 from the 10 cases were at the age of 65–87 years it seems that advanced age has no influence on expression of the investigated proteins. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640

18

Electrospun nanofibrous nets as a potential materials for neurology

45%

Kowalczyk T., Sulejczak D., Frontczak-Baniewicz M., Grieb P., Kowalewski T. A.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr 1

Electrospun nanofibers are very promising material to be used in biomedicine. Electrospinning (electrical spinning) is a method of producing non-woven fibers of diameters down to 2 nm (and length of many cm) in contrast to a classical spinning - not thinner than 5µm. Main feature of the nanofibers is a very high surface to volume ratio of the material and lack of crystalline defects. The electrospinning process is usually conducted in solvents, even water can be applied, the process conditions are in favor to a very soft molecules and species. Such made fibers contain undamaged polymers or drugs, the proteins are not denaturated even living cells can survive the process. Mats made of the fibers are done of variety of polymers, including biodegradable polyesters and proteins. They can be used as scaffolds for the tissue engineering, wound dressings, barrier materials or Drug Delivery Systems (DDS). The main advantage for the use of mats for the tissue engineering is size similarity of the nanofibers and the fibers of Extracellular Collagen Matrix (ECM). For the use as DDS the fibers act as “nanodiffusion pump” releasing constant amount of drug in a controlled and tailored manner. Electrospun nanofibers made of biodegradable and biocompatible polymers(materials) are harmless and safe nanomaterials. They don’t cause inflammatory reaction when implanted. They can be used either to help guiding cells to produce properly formed tissues or inhibit cells growth to prevent liaisons. Depending of the type of material used, processing, surface modification, even the way of sterilization material of desired properties may be produced. The fibers already tested in our laboratories were successfully used as a scaffolds for cells growth (human: UCSC, MSC, hepatocytes). Other applications included: coatings for Bioglass bone implants, nanofibrous sensors made of BSA surface modified by FITC and conductive nanofibers. Research on anti -liasions, wound dressing, barrier materials and tubular scaffolds of enhanced vascularization are being conducted. Supported by the project of Polish Ministry of Science and Higher Education nr NR13-0081-10.

19

Overexpression of P2X7R and early activation of cerebral microglia during experimental autoimmune encephalomyelitis

45%

Grygorowicz T., Sulejczak D., Rafalowska J., Lenkiewicz A., Struzynska L.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

|

nr S

Multiple sclerosis (MS) is an autoimmune, neurodegenerative disease which is one of the most frequent reasons of disabilities of young adults and a serious problem for modern medicine due to the unknown etiology. Experimental autoimmune encephalomyelitis (EAE) is a commonly used rodent model of MS. EAE is evoked by immunization of female Lewis rats with homogenate of guinea pigs’ spinal cord combined with complete Freund’s adjuvant and inactivated Mycobacterium tuberculosis. It is well known that during the development of MS and EAE, the immune system sensitizes against self myelin and the permeability of blood-brain barrier (BBB) increases what enables an inflow of immune cells into the central nervous system. The immune system attacks and destroys myelin in the brain and the spinal cord what further leads to degeneration of neurons. The aim of the study was to investigate the time-window of microglial activation, the level of proinflammatory cytokines (IL-1, IL-6, TNFα) and the status of BBB in the early stages of EAE. We correlated the results with the microglial and endothelial expression of purinergic P2X7 receptor which is known to play a role in inflammation due to a release of proinflammatory mediators. The results of microscopic analysis revealed the increased permeability of BBB. At day 2 and 4 p.i. we also observed decreased expression of claudin5 protein which is an important marker of BBB tightness. However, starting from day 6 p.i. we noticed significant upregulation of this protein expression. The early activation of microglial cells at day 4 post immunization (dpi), in asymptomatic phase of the disease, together with an increased level of proinflammatory cytokines were observed. These changes correlated temporary with overexpression of P2X7R which was noticed on microglial cells and pericytes of blood vessels in brains of EAE rats. The results suggest the critical role of this receptor in early events during EAE development.

20

Neurons and glia npregulate FIk1 following various cortical injuries

39%

Sulejczak D., Nosecka E., Macias M., Skup M., Czarkowska-Bauch J., Walski M., Frontczak-Baniewicz M.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

Ograniczanie wyników

Apoptoza i metody jej identyfikacji.

Temporal changes in Bel-2 and Bax proteins in rat cerebral cortex following devascularizing lesion

Axoplasmic localisation of the NFkappaB p65 subunit in the rat brain

Selected biochemical characteristics of the rat mhSOD1(G93A) transgenic model of familial amyotrophic lateral sclerosis (fALS) and the effects of cytidine 5-diphosphocholine (sodium salt, CDPch) treatment

Expression of purinergic P2X(7) receptor in rat brain during the symptomatic phase of experimental autoimmune encephalomyelitis and after recovery of neurological deficits

Phenotypes of cell pools populating the injury site in a rat model of surgical brain cortex lesion

Diversity of immunophenotypes of endothelial cells participating in new vessel formation following surgical rat brain injury

Endothelial progenitor cell in newly-formed capillaries following surgical brain injury of rat cerebral cortex

Zwierzęcy model lipopolisacharydowego zapalenia płuc

Neurovascular unit and glial scar formation following the surgical brain injury

Surgical injury-induced early neocortical microvascular changes and characteristics of the cells populating the peri-lesion zone

Glial expression of purinergic P2X7 receptor in rat brain during the course of experimental autoimmune encephalomyelitis

Dootrzewnowe podanie 2-deoksyglukozy - szczurzy model glukodeprywacji mózgowej

Unilateral photothrombotic stroke in the frontal cerebral cortex causes biiateral impairment of skilled movements of the rat forelimb

Astroglial reaction in the early asymptomatic phase of experimental autoimmune encephalomyelitis

Distribution of TrkB receptors in motor-sensory cortical areas in the rat

Immunoexpression of the selected compounds of the SMN complex in spinal cord neurons in patients with sporadic amyotrophic lateral sclerosis (sALS)

Electrospun nanofibrous nets as a potential materials for neurology

Overexpression of P2X7R and early activation of cerebral microglia during experimental autoimmune encephalomyelitis

Neurons and glia npregulate FIk1 following various cortical injuries