Wyniki wyszukiwania

1

Ultrastructural features of the neurovascular unit in Alzheimer's neurodegeneration

100%

Frontczak-Baniewicz M., Walski M.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

91-96

Recent studies suggest that capillaries, neurons, and astrocytes form a functional unit that serves to maintain cerebral homeostasis. Physiological interactions between all these components of the neurovascular unit control cerebral microcirculation, while abnormal regulatory mechanisms lead to cerebral dysfunction and disease states, such as Alzheimer’s disease (AD). Using electron microscopy, we studied a fragment of the frontotemporal cortex obtained intraoperatively from a patient with established AD. The objective of our study was to assess the ultrastructure of the components of the neurovascular unit. Such ultrastructural studies allow analyzing the structural process of new blood vessels formation and also the appearance of neurons and astrocytes contributing to the neurovascular unit. We suggest that dysfunction of particular components of the neurovascular unit underlies AD and ultimately leads to neurodegeneration.

2

Mozgowe naczynia kapilarne. Ultrastrukturalne wykladniki procesow angiogenezy

100%

Frontczak-Baniewicz M., Walski M.

Postępy Biologii Komórki

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2004

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tom 31

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nr 3

563-573

3

Glial scar instability after brain injury

100%

Frontczak-Baniewicz M., Walski M.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

97-102

Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.

4

New vessel formation after surgical brain injury in the rat's cerebral cortex. I. Formation of the blood vessels proximally to the surgical injury

100%

Frontczak-Baniewicz M., Walski M.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 2

5

Conjugation-specific cortical reorganization during zygocyst formation in the hypotrich ciliate Paraurostyla weissei

100%

Frontczak-Baniewicz M., Jerka-Dziadosz M.

Acta Protozoologica

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1992

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tom 31

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nr 2

6

New vessel formation after surgical brain injury in the rat's cerebral cortex. II. Formation of the blood vessels distal to the surgical injury

100%

Walski M., Frontczak-Baniewicz M.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 2

7

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

81%

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

8

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

81%

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

9

Neurovascular unit and glial scar formation following the surgical brain injury

81%

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

10

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

81%

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.

11

Oxidative stress and inflammatory response in rat brain and live R following oral administration of silver nanoparticles

81%

Skalska J., Frontczak-Baniewicz M., Lenkiewicz A., Struzynska L.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

BACKGROUND AND AIMS: Silver nanoparticles (AgNPs) are one of the most important class of nanomaterials used in a wide range of medical and industrial applications. However, the information about their toxicity to mammalsislimited. The aim of thisstudy was to investigate the effect of oral exposure to AgNPs on brain and liver of rats. The deposition of silver nanoparticles in these organs has been shown to induce hepatotoxicity and neurotoxicity. These toxic effects may include oxidative stress with subsequent inflammatory response. METHODS: Wistar rats were exposed orally to AgNPs (10±4 nm in diameter) or silver ions at a dose of 0.2 mg AgNPs or Ag+/ kg bw for 14 days. Then all animals were sacrificed 24 h after last exposure and tissues were collected for further studies. RESULTS: The presence of AgNPs in brain tissue was confirmed by using TEM technique. The level of free radicals and end-products of lipid peroxidation increased in both organs after exposure to both, silver nanoparticles or silver ions. However, the changes in inflammatory markers (based on IL-1β, IL-6 and TNF-α relative protein levels) were not statistically significant. CONCLUSIONS: These results show that following AgNPs or silver ions administration, oxidative stress is induced in brain and liver tissues. However, it seems that the time of exposure to both of silver forms was too short to cause the inflammatory response.

12

Ultrastructural evaluation of phagocytic function of perivascular cells and interstitial microglia in the brain of rats surviving one year after cardiac arrest-induced global cerebral ischemia

81%

Walski M., Frontczak-Baniewicz M., Wojewodzka U., Gajkowska B.

Acta Biologica Cracoviensia. Series Zoologia

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2003

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tom 45

13

Translocation of apoptosis-related proteins in MCF-7 cells exposed to camptothecin in the mitochondrial pathway of apoptosis

81%

Gajkowska B., Wojewodzka U., Walski M., Frontczak-Baniewicz M.

Acta Biologica Cracoviensia. Series Zoologia

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2003

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tom 45

14

Photochemically-induced vascular damage in brain cortex. Transmission and scanning electron microscopy study

81%

Gajkowska B., Frontczak-Baniewicz M., Gadamski R., Barskov I.

Acta Neurobiologiae Experimentalis

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1997

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tom 57

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nr 3

15

Effects of staphylococcal alpha-toxin on the ultrastructure of the rat hypothalamo-neurohypophyseal system

81%

Gajkowska B., Gadamski R., Frontczak-Baniewicz M.

Acta Neurobiologiae Experimentalis

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1994

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tom 54

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nr 3

16

Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope

81%

Walski M., Chlopicki S., Celary-Walska R., Frontczak-Baniewicz M.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Human atherosclerotic plaque morphology at its various stages was extensively documented using light microscopy. However, much less is known of the ultrastructure of the human atherosclerotic plaque, in particular of ultrastructure of endothelial cells in atherosclerosis. Here, we analysed alterations of endothelial cells covering advanced atherosclerotic plaque in carotid artery using scanning electron microscope. Examination was performed on specimens from atherosclerotic lesions of the interior carotid artery, collected from 8 patients who had undergone endarterectomy. We found wide spectrum of pathological alterations of the luminal surface of atherosclerotic plaque. In dominant part of the vessel, endothelial layer was preserved but displayed pronounced irregularities in endothelial architecture including appearance of cuboidal cells. Some endothelial cells were covered by numerous microvilli and/or contained "craters" disrupting continuous surface of the endothelium. Platelets and leukocytes adhering to endothelium were frequently observed. There were also areas of the vessel lumen with endothelial denudation, in which the subendothelial surface containing fibrin proteins and collagen fibrils were visible. Interestingly, signs of proliferation of endothelial cells tending to cover the partially denuded vessel were observed. In summary, in scanning electron microscope, preserved endothelial cells of advanced atherosclerotic plaque displayed pronounced pathology; whether any of these changes represent the ultrastructural correlate of endothelial dysfunction remains to be established.

17

Electrospun nanofibrous nets as a potential materials for neurology

71%

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.

18

The influence of silver nanoparticles on blood-brain barrier function and morphology in adult rats

71%

Sulkowski G., Dabrowska-Bouta B., Orzelska-Gorka J., Frontczak-Baniewicz M., Struzynska L.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: Neurotoxicity of silver nanoparticles has been confirmed in a lot of in vitro and in vivo studies using different experimental models. However, the mechanisms of the toxic action have not been fully clarified. Since nanoparticles have the ability to enter the brain and significantly accumulate in this organ, it is important to investigate their neurotoxic mechanisms. AIM(S): We examined the effect of prolonged exposure on blood-brain barrier (BBB) ultrastructure and expression of tight junctions protein components as opposed to the ionic silver. METHOD(S): In the current study we exposed adult rats to a low dose (0.2 mg/kg b.w.) of small (10 nm) citrate-stabilized silver nanoparticles (AgNPs). RESULTS: The BBB is a highly specialized structure composed of a basement membrane and microvascular endothelial cells which interact with pericytes, perivascular artrocytes and neurons forming neurovascular unit. Administration of AgNPs over a two-week period resulted in changes in BBB ultrastructure and integrity. TEM analysis revealed accumulation of AgNPs inside endothelial cells of microvessels, mainly in lysosomes. Ultrastructural features of enhanced permeability of cerebral microvessels were observed such as enhanced activity of pinocytotic vesicular system and swollen perivascular astrocytic end-feets. This suggests uptake of fluid and its transfer to parenchyma which further results in perivascular edema. Additionally, we observed changes in the level of mRNA of the main tight junction proteins such as claudine, ocludine, and ZO1 as well as PDGF and its receptor PDGFbR which constitute the signaling pathway between endothelial cells and pericytes. All these characteristic protein components are responsible for the integrity of BBB. CONCLUSIONS: The results of the current study demonstrate that exposure of adult rats to AgNPs induces BBB dysfunction leading to the enhanced permeability of cerebral microvessels.

19

Maternal immune activation during pregnancy alters the expression of mitochondrial dynamics markers in the brain of rat offspring

71%

Zawadzka A., Cieslik M., Gewartowska M., Frontczak-Baniewicz M., Adamczyk A.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

INTRODUCTION: Prenatal exposure to infection and subsequent inflammatory responses, as well as, mitochondrial dysfunction has been implicated in the pathogenesis of autism spectrum disorders (ASDs). However, the molecular links between infection-induced fetal brain changes, mitochondrial deregulation, and the autistic phenotype remain obscure. AIM(S): Analysis of maternal immune activation (MIA)-induced changes in the expression of mitochondrial dynamics markers in the brain of the neonatal and adolescent rat offspring. METHOD(S): The MIA model was induced by single intraperitoneal injection of lipopolysaccharide (100 μg/kg b.w.) to pregnant rats at embryonic day 9.5. On the 7th or 52-53rd post-natal day, rat offspring were decapitated, and the brains isolated. Transmission electron microscopy (TEM), quantitative real‑time PCR (qPCR), and immunoblotting were used to determine mitochondrial ultrastructure and mRNA/protein expression, respectively. RESULTS: The electron microscopic study demonstrated altered mitochondrial morphology, including fragmented cristae, expanded matrix compartment, and membrane disruption in both the cerebral cortex and hippocampus of adolescent MIA offspring. Moreover, changes were noted in the expression of proteins involved in the maintenance of mitochondrial morphology. We observed upregulated fusion machinery proteins – mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and Opa1 – as well as mitochondrial fission proteins – dynamin related protein‑1 (Drp1) and fission protein 1 (Fis1) – in the neonatal MIA brains. However, in adolescent animals exposed to prenatal infection, the expression of Mfn1, Mfn2 and Opa1 was significantly reduced; nevertheless, Drp1 and Fis1 remained increased CONCLUSIONS: MIA-evoked perturbations in the proteins regulating mitochondrial dynamics reveal potentially important aspects of the mechanism linking neuroinflammation, impaired mitochondrial function, and ASD. FINANCIAL SUPPORT: Supported by the POWER Och!Doc Program and NSC grant 2016/23/D/NZ4/03572.

20

Expansion of the Golgi apparatus in rat cerebral cortex following intracerebroventricular injections of streptozotocin

71%

Grieb P., Kryczka T., Fiedorowicz M., Frontczak-Baniewicz M., Walski M.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

|

nr 4

Ograniczanie wyników

Ultrastructural features of the neurovascular unit in Alzheimer's neurodegeneration

Mozgowe naczynia kapilarne. Ultrastrukturalne wykladniki procesow angiogenezy

Glial scar instability after brain injury

New vessel formation after surgical brain injury in the rat's cerebral cortex. I. Formation of the blood vessels proximally to the surgical injury

Conjugation-specific cortical reorganization during zygocyst formation in the hypotrich ciliate Paraurostyla weissei

New vessel formation after surgical brain injury in the rat's cerebral cortex. II. Formation of the blood vessels distal to the surgical injury

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

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

Oxidative stress and inflammatory response in rat brain and live R following oral administration of silver nanoparticles

Ultrastructural evaluation of phagocytic function of perivascular cells and interstitial microglia in the brain of rats surviving one year after cardiac arrest-induced global cerebral ischemia

Translocation of apoptosis-related proteins in MCF-7 cells exposed to camptothecin in the mitochondrial pathway of apoptosis

Photochemically-induced vascular damage in brain cortex. Transmission and scanning electron microscopy study

Effects of staphylococcal alpha-toxin on the ultrastructure of the rat hypothalamo-neurohypophyseal system

Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope

Electrospun nanofibrous nets as a potential materials for neurology

The influence of silver nanoparticles on blood-brain barrier function and morphology in adult rats

Maternal immune activation during pregnancy alters the expression of mitochondrial dynamics markers in the brain of rat offspring

Expansion of the Golgi apparatus in rat cerebral cortex following intracerebroventricular injections of streptozotocin