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Morphological changes in the peripheral nervous system in the case of congenital malformations of the spinal cord

100%

Drac H., Pniewski J., Rafalowska J.

Acta Neurobiologiae Experimentalis

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1992

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tom 52

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nr 3

2

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

88%

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

3

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

88%

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

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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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.

4

Possible role of microvessel-located P2X7R in BBB function during the course of EAE

76%

Grygorowicz T., Rafalowska J., Lenkiewicz A., Chrzanowska H., Wojda R., Szopinski R., Struzynska L.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Multiple sclerosis is a serious problem of medicine and one of the most frequent reasons of disabilities of young adults. EAE is a commonly used rodent model of MS. In physiological conditions the blood-brain barrier (BBB) maintains CNS homeostasis and prevents uncontrolled inflow of immune cells from the blood circuit. During the development of EAE, damaged BBB fails to protect CNS from autoreactive immune cells. In this study we try to investigate a possible role of P2X7R in pathological changes of BBB during EAE. Analyzing BBB tightness we observed decreased expression of Claudin5 (protein component of tight-junctions) in the isolated microvessels’ fraction using western blot technique. These data were confirmed by immunofluorescence staining of brain sections against Claudin5. To assess functional state of BBB we carried out immunohistochemical staining against albumin and we observed its extravasation in early phase of EAE. All these data suggest dysfunction of BBB at the early stage of the disease. In parallel we observed overexpression of P2X7R in microvessels’ fraction and noticed correlation between its expression and increased BBB permeability using antagonist of P2X7R. Supported by grant nr: 2012/05/N/NZ4/02191

5

Arginine and tetrahydrobiopterin supplementation in rats with salt-induced blood pressure increase: minor hypotensive effect but improvement of renal haemodynamics

76%

Kuczeriszka M., Walkowska A., Olszynski K. H., Rafalowska J., Sadowski J., Kompanowska-Jezierska E.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 2

6

Is SMN immunoexpression in hypertrophied Nisl granulations in amyotrophic lateral sclerosis a morphological equivalent of reinnervation ?

76%

Dziewulska D., Sulejczak D., Gogol A., Gogol P., Ogonowska W., Modrzewska-Lewczuk M., Rafalowska J.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr Suppl.1

Reinnervation observed in early stage of amyotrophic lateral sclerosis (ALS) is a compensatory mechanism for motoneuron loss. Since survival motor neuron (SMN) protein could be involved not only in neuroprotection but also in the transport of mRNAs in motoneuron axons, we examined its immunoexpression in anterior horn motoneurons of ALS patients with reinnervation in EMG. SMN immunolabel was observed in neuron cytoplasm and neurities but it was particularly intense in enlarged Nissl granules. This finding may mirror increased synthesis of the protein in rough endoplasmic reticulum being not only an attempt of motoneuron to selfprotection but also necessary for nerve sprouting. Study supported by the Ministry of Sciences and Higher Education grant NN 401 014 640.

7

The protective effect of CDP-choline on neuronal changes in a model of slow glutamate excitotoxicity in vitro

76%

Naganska E., Matyja E., Taraszewska A., Rafalowska J., Grieb P., Zielinska M.

Acta Neurobiologiae Experimentalis

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2006

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tom 66

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nr 4

8

Immunoreactivities of some proteins forming SMN protein complex within spinal cord in rat model of fALS

76%

Rafalowska J., Sulejczak D., Gadamski R., Wojda R., Mordzewska-Lewczuk M., Dziewulska D.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Introduction: Amyotrophic lateral sclerosis (ALS) is a major neurodegenerative disease to afflict the adult human population. ALS causes a progressive motoneuron degeneration within anterior horns of the spinal cord. Recent data indicate the presence of mutations in the SMN (Survival Motor Neuron) gene that cause a deficits in the level of the functional SMN protein and may be an exacerbating factor in the disease development of rat model of fALS. SMN forms the multiprotein complex with selected gemins (i.a. gemin 2, 3 and 4). It is known, that the complex is important for motoneuron development in ontogenesis as well as in the proper functioning of mature motoneuron. However, the level of the SMN and individual gemin expression during the life both in humans and rats still become uncovered. The aim of our study was to determine the immunoreactivities of SMN and gemins 2, 3 and 4 in rat model of fALS during all life span. Material and method: Male rats mutated in SOD-1 were subjected to experiments. Animals at age of 60 days (group 1), 90 days (group 2), 120 days (group 3) were asymptomatic. The last group involving symptomatic rats was created from animals older than 120 days. Rats were perfused in deep anaesthesia. The spinal cords were removed and processed in routine histological staining techniques as well as in immunohistochemical methods (to detect SMN and selected gemins proteins). Labelling sections of spinal cords were analyzed with light and fluorescent microscope. Result: SMN and all investigated gemins were present in spinal cord motoneurons in rats from all experimental groups. However, the level of staining was weaker in the paretic rats. In the opposition to other examined proteins the immunoreaction of gemin 2 was weaker starting from 90 day of life. Conclusion: The SMN protein complex is present in motoneurons within the spinal cord during all animal lifespan in the rat model of familiar ALS. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640

9

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

64%

Kozniewska E., Michalik R., Rafalowska J., Gadamski R., Walski M., Frontczak-Baniewicz M., Piotrowski P., Czernicki Z.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

145-160

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.

Ograniczanie wyników

Morphological changes in the peripheral nervous system in the case of congenital malformations of the spinal cord

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

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

Possible role of microvessel-located P2X7R in BBB function during the course of EAE

Arginine and tetrahydrobiopterin supplementation in rats with salt-induced blood pressure increase: minor hypotensive effect but improvement of renal haemodynamics

Is SMN immunoexpression in hypertrophied Nisl granulations in amyotrophic lateral sclerosis a morphological equivalent of reinnervation ?

The protective effect of CDP-choline on neuronal changes in a model of slow glutamate excitotoxicity in vitro

Immunoreactivities of some proteins forming SMN protein complex within spinal cord in rat model of fALS

Mechanisms of vascular dysfunction after subarachnoid hemorrhage