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D Maślińska

Publications and source records attributed to D Maślińska.

At least 19 recordsLinked to original sources

Expression of IL-15 and IL-15 receptor isoforms in select structures of human fetal brain.

IL-15, a key cytokine linking innate and acquired immunity, is expressed in many cell types and tissues. Recent data indicate constitutive expression of IL-15 in human neural cell lines and tissues. The aim of the present study was to examine the expression patterns of mRNA encoding IL-15 and IL-15 receptor alpha (IL-15Ralpha) isoforms in select structures of human fetal brain. We report that mRNA for IL-15 and IL-15Ralpha isoforms were expressed in all tested brain structures: cerebral cortex, cerebellum, hippocampus, and thalamus. However, the levels of IL-15 and IL-15Ralpha mRNA were higher in the hippocampus and cerebellum in comparison with cortex and thalamus. Moreover, higher levels of cytosol in comparison with membrane-bound IL-15 isoform were present in all brain structures. The constitutive, but distinct, expression of IL-15 and its receptors in select human fetal brain structures suggests that IL-15 plays a role in their development and physiology.

Brain↗

The cytokine network and interleukin-15 (IL-15) in brain development.

Cytokines are heterogeneous peptide molecules, produced by a variety of cells of immune and non-immune origin. Cytokines mediate a wide range of biological activities through a functional network, which they create. Cytokines utilise the complex receptor system, which includes a receptor subunit specific for each cytokine and common receptor subunits shared by cytokines which are members of the principal receptor family. After cytokine binding to a specific membrane receptor on target cells, a series of signal transduction pathways are stimulated. This may lead to translocation to the nucleus of phosphorylated signal transducers and activators of transcription (STAT) with up-regulation of the transcription and/or expression of new genes. Peripheral cytokines (e.g. interleukins) may enter the central nervous system in areas that lack a tight blood-brain barrier and/or by active transport. However, during systemic inflammation the brain is modulated not only by cytokines originated in peripheral organs but also by cytokines synthesised by the brain cells. Cytokines produced in the brain may influence its development, differentiation and function in normal and pathological circumstances. The recent description and characterisation of IL-15 indicate that this cytokine plays a pivotal role in inflammatory events. IL-15 binds to a receptor that possesses a unique alpha chain but utilises also the beta and gamma chains of the IL-2R to transduce signals in target T cells. In mast cells, IL-15 utilises a novel specific receptor IL-15RX. The IL-15 gene is constitutively expressed in the nerve tissue and during differentiation of neurons two distinct isoforms of IL-15 mRNA have been found. Results of our study provide the evidence that in the normal brain IL-15 is present only in neurons but glial cells contain this cytokine only when they are activated/transformed by inflammatory insults.

Aging↗

Mast cells in the mouse mammary gland--correlation with the development of lactiferous structures.

Specimens of mouse mammary glands obtained from animals being in different phases of reproductive cycle were collected. After staining MCN, the total mast cell area (TMC), mean mast cell area (MMC), and lactiferous structure density index (LDI) were examined in sections, using a computer image analysis system. Statistically significant (P < 0.05) results were: 1. An increase in MCN observed in Group I (4-5 and 9-10 days of pregnancy), a decrease in MCN observed in Group II (2nd and 10th day of lactation); 2. Changes of TMC fully corresponding to changes of MCN; 3. Increase in MMC observed in Group I at mid (days 9-10) and at the end (days 18-19) of pregnancy, decrease in MMC observed in Group IIB (10th day of lactation); 4. LDI (%) higher at the end of pregnancy (Group IC) and during lactation (groups IIA, IIB), compared with control (23.5 +/- 4.12, 37.6 +/- 3.24, 71.0 +/- 4.33 vs. 3.8 +/- 0.39). The observed changes in the number and size of MC strictly correspond to physiological phenomena leading to alternation of the mouse mammary gland functional status by development/involution of the lactiferous structures.

Alcian Blue↗

Expression of cyclooxygenase-2 in astrocytes of human brain after global ischemia.

COX-2 expression, an inducible form of cyclooxygenase was studied in human brain after ischemia-reperfusion. Previously, a prominent COX-2 upregulation was described in neurons few hours or days after ischemia but little is known about COX-2 expression in non-neuronal cells participating in post-ischemic inflammation. Aim of the study was to examine COX-2 expression in activated glial cells of individuals, who died two or more weeks after resuscitation. In the cerebral cortex of these individuals ischemic necrosis was more or less widespread. In some brain areas numerous microglial cells were found. At the centre of the necrosis high expression of COX-2 was detected in macrophages, polymorphic cells and leukocytes. At the margin of necrosis hypertrophic astrocytes were COX-2 immunopositive. Expression of COX-2 was observed also in the wall of blood vessels of necrotic brain areas and in meninges. The results of the study suggest that in the late period after global ischemia reactive and hypertrophic astrocytes and macrophages may be the major sources of prostaglandins in the human brain.

Adult↗

Phenotype of mast cells in the brain tumor. Capillary hemangioblastoma.

Mast cells (MC) are heterogenous cell population. In normal human brain they are not numerous. Increases in number of mast cells within CNS occur in certain disease states including neoplasms. In capillary hemangioblastoma several authors reported mast cells as a fourth cell type of the tumor. The aim of the present study was to examine phenotype and distribution of MC in cerebellar capillary hemangioblastoma by means of specific immunological markers. Study was performed on the tumor of ten affected individuals. Tumor specimens of seven cases were fixed in formalin and embedded in paraffin wax. Additional three tumours were fresh-frozen samples. Mast cells were identified with two monoclonal antibodies generated against tryptase and chymase. In all capillary hemangioblastomas mast cells were numerous exclusively in the tumor mass and only occasionally found in adjacent or far from the tumor located areas of the cerebellum. The cells contained tryptase and chymase. At periphery of hemangioblastomas some mast cells underwent degeneration and calcification. Our results confirm previous observations that mast cells are numerous in the capillary hemangioblastoma and show that most of these cells are tryptase/chymase phenotype (MCTC).

Brain Neoplasms↗

Constitutive expression of cyclooxygenase-2 (COX-2) in developing brain. A. Choroid plexus in human fetuses.

It is believed that prostanoids produced by COX-1 activity are essential for the physiological functions of tissues while those produced by COX-2 lead to various pathological changes in these tissues. Brain is an exceptional organ where in some neurons COX-2 mRNA and its protein are constitutively expressed. Since some prostaglandins may play an important role in the control of blood-brain barrier and cerebral blood flow the purpose of the present study was to examine the COX-2 expression in choroid plexus, which participate in the nutrition of brain parenchyma of human fetuses. Study was performed on 25 brains of human fetuses from 12 to 38 weeks of gestation. In light and electron microscopy characteristic developmental transformation of choroid morphology was observed. In young fetuses from 12 to 20 week of gestation epithelial cells of choroid plexus are cuboidal, contain large amount of glycogen storage and their nuclei are COX-2 immunopositive. From 25 week of gestation until term the amount of glycogen in the choroid plexus diminishes, some apical nuclei are shifted toward central parts of the cells and number of cytoplasm organelles increases. In these cells expression of COX-2 protein is located in cytoplasm but epithelial nuclei are immunonegative. Our results provided evidence that COX-2 is constitutively expressed in the developing human choroid plexus. Different localization of COX-2 in choroid epithelial cells suggests that this enzyme may play a different role in various periods of the choroid plexus development.

Choroid Plexus↗

Some aspects of the inflammatory process.

The inflammatory process is a nonspecific complex, stereotype, coordinated response of tissues to injury. This process involves vascular permeability, active migration of blood cells, and passage of plasma constituents into the injurious tissue. The molecules that mediate the initial events of inflammation are the adhesion molecules. They are localized on leukocytes and endothelium. The adhesion and cell-cell cooperation appear to be critical for the migration of leukocytes to the abluminal surface of the blood vessels. The emigrating cells initiate the complex reactions that are controlled by a multitude of intercellular messengers called mediators. Prostanoids, that are products of arachidonic acid metabolism in cyclooxygenase pathway are involved in the process of communication between cells. Two isoforms of the cyclooxygenase COX-1 and COX-2 were found. They subserve different physiological function largely because of the striking differences in their tissue expression and regulation. A common feature of chronic inflammation is the persistence of a large number of leukocytes in the tissue; thus, their removal is important for the resolution of the inflammatory process. The mechanism by which they are removed includes the apoptotic recognition system. The new concepts regarding the therapy of the diseases concomitant with inflammatory reaction should include the inhibition of the appropriate isoform of cyclooxygenase and the regulation of apoptotic process in some cells.

Animals↗

Morphological forms and localization of microglial cells in the developing human cerebellum.

There are relatively few studies on microglia of human developing brain thus function and location of these cells at this period of life are unknown. Moreover, all of them concentrated on the cells in very early period of fetal life. To achieve further insight into the participation of microglial cells in the development of the central nervous system the brains of fetuses, newborns and infants were examined by means of immunological markers: Ricinus communis agglutinin-1 (RCA-1) and ferritin antiserum. Brains of 12 fetuses and infants ranging in age from 14 weeks of gestation to 5 months after birth were used in the study. The fetuses were derived following spontaneous abortions. In pre-term and term newborns the cause of death was of maternal origin (placental insufficiency) or accidental sudden death. Coronal blocks of cerebellum cut into 5 microns thick sections were used in the study. The developing microglial cells were detected by both markers (RCA-1 and anti-ferritin). Ricinus communis agglutinin recognizes carbohydrate residues on the surfaces of microglial and endothelial cells. Therefore, in the sections incubated with this lectin brain vessels as well as microglia were visualized. The second microglial marker anti-ferritin serum detected precisely all morphological subpopulations of microglia including ameboid and ramified cells but endothelial cells remained immunonegative. Therefore, in 14 weeks of gestation only round ameboid microglia were ferritin-immunopositive in cerebellum. These cells were localized at the periphery of the periventricular, germinal matrix and were surrounding a group of nerve cells of the developing dentate nucleus. In 16 week-old fetuses ameboid cells were present in the hilus and between gyri of the dentate nucleus. The ferritin-positive microglial cells on the convolutions of the dentate nucleus gyri manifested as the cells with short fine branched processes and scanty cytoplasm. In cerebellum of the 20 week-old fetuses the subpopulation of branched (ramified) microglia were more numerous than ameboid cells. Ameboid cells were present mainly in the intermediate zone of the future white matter and ramified cells penetrated the inner (at the one third of its thickness) part of the developing internal granular layer of cerebellar cortex. The upper part of cerebellar cortex was colonized by microglia between 24-28 weeks of gestation. In cerebellum of fetuses over 28 weeks of gestation numerous microglial cells infiltrated mainly the Purkinje cell layer, first in the vermis, later in the hemispheres. From 36 weeks of gestation to the birth ferritin-immunopositive microglial cells gradually disappeared from the cerebellar cortex. The microglia of the term newborns and of a 5 month-old child manifested mainly as ramified cells located in the white matter. The results of our study lead to the conclusion that the localization of microglial cells in the brain structure and their morphological forms correlate precisely with the appropriate stages of the brain development.

Cell Death↗

Beta-protein immunoreactivity in the human brain after cardiac arrest.

Brain of twelve, 44-78 years old non-demented patients affected by total ischemia after cardiac arrest, were used in the study. All of them were resuscitated within a few minutes after cardiac arrest and they survived for 3 to 36 days afterward. In all cases, after cardiac arrest, beta PP overexpression was found by immunocytochemical methods in many cortical and subcortical neurons as well as in ependymal and choroid plexus cells. This overexpression of beta PP, was concomitant with formation of many A beta nonfibrillar (thioflavine-negative) plaques in the neuropil. Because of a break in the blood-brain barrier around many vessels, weakly A beta-immunoreactive material was also found. The data presented provided strong evidence that the total brain ischemia resulting from cardiac arrest is a risk factor for beta-amyloidosis.

Adult↗

DNA fragmentation and ultrastructural changes in the brain of rabbits treated with vincristine.

Numerous anticancer drugs, which are in current use, have been shown to induce apoptosis in susceptible cells of some tissues. The aim of the study was to examine whether vincristine injected parenterally to rabbits may affect DNA and ultrastructure of cells in the brain. Vincristine 0.25 mg/kg of body weight was injected to immature (seven day-old) and adult (90 day-old) rabbits. Two, four and six hours after treatment, the significant increased number of cells with internucleosomal fragmentation of DNA was found. At the same time, in some glial cells characteristic for apoptosis condensation of chromatin was observed. Numerous apoptotic bodies were scattered throughout the tissue or digested by neighboring cells (astroglia, oligodendroglia, microglia and pericytes). The result provided evidence that vincristine treatment may induce apoptosis and trigger phagocytic clearance of apoptotic bodies in the brain. Presumably, both of these processes participate in neurotoxic effect of the drug on the CNS during chemotherapy.

Animals↗

The features of peripheral nerve lesions in young and adult rabbits after vincristine administration.

The comparison of neuropathological picture of vincristine induced neuropathy immediately after the end of its administration and after three months of survival was performed. The adult rabbits and six litters of newborns received vincristine once a week in increasing doses 0.05-0.25 mg/kg of body weight. The early changes consisted in degeneration of axons and myelin sheaths and lesions of the Schwann cells. The features of changes allow to suspect that vincristine may induce, in addition to the well known primary axonal damage, a toxic effect on the Schwann cells with secondary damage of myelin sheaths. The changes were more severe in adults than in young animals. The observations after three months of survival allow to think that the administered doses of vincristine did not impede the improvement when treatment was interrupted.

Age Factors↗

Ultrastructure of brain vessel in vincristine treated rabbits.

Ultrastructure of the brain blood vessels has been examined in rabbits treated with a single intraperitoneal injection of vincristine (VCR). The results provided evidence that some microvessels in these animals undergo vasoconstriction concomitant with projection of numerous endothelial microvilli into the vessel lumen. Vasoconstriction was followed by microvessel loss of regular shape and degeneration of some endothelial cells resulting in the digestion of apoptotic bodies by perivascular pericytes. Most of those changes (eg. vasoconstriction) appeared transient and were not observed seven days after treatment.

Animals↗

Apoptosis, programmed cell death in the central nervous system.

Cell death by apoptosis occurs in a number of normal tissue systems including the nervous system. It is a highly specific process, which requires new gene expressions and the production of new proteins. The genetic information determines biochemical and morphological sequence of events in the cell undergoing apoptosis. This review focuses on the recent informations concerning the participation of the genes in the survival and death of neurons in the central nervous system and the effect of the anti-cancer drugs on the induction of apoptosis in the cell.

Animals↗

Overexpression of amyloid precursor protein of Alzheimer's type in brains of intoxicated children.

The coincidence of neuronal stress induced by intoxication and an overexpression of amyloid precursor protein (APP) in the brains of children was examined. Brains of ten children accidentally intoxicated by poisonous mushroom were studied by means of immunohistochemical methods using monoclonal antibodies generated against different domains of APP and glial cell markers. Overexpression of APP was found in the brain neurons of all intoxicated children. Neurons were immunopositive with the antibodies generated against the middle (amyloid beta protein) domain of APP. No extracellular deposits were found in the tissue. Our results provided, for the first time, the evidence that overexpression of APP concomitant with the neuronal stress is age-independent phenomenon appearing not only in the brain of adults but in very young individuals as well.

Alzheimer Disease↗