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Biomedical subjects

F Joó

Publications and source records attributed to F Joó.

At least 37 records · Page 2Linked to original sources
PubMed1996

Endothelial cells of the brain and other organ systems: some similarities and differences.

The cerebral endothelium represents an active interface between blood and central nervous system. The blood-brain barrier restricts the free passage of nutrients, hormones, drugs and cellular elements to the brain. Recent studies performed on freshly isolated cerebral microvessels and cultured endothelial cells of brain capillaries provided a better understanding of the properties and functions of cerebral endothelial cells. This review summarizes the main findings of the in vitro approach in the blood-brain barrier research, describes the common endothelial and unique cerebral features of the brain endothelium, and provides a short overview on how these blood-brain barrier characteristics can be induced in cerebral endothelial cells by the neighbouring cells.

Blood-Brain Barrier↗
PubMed1996

Cultured vascular endothelial cells of the brain.

The endothelium is a single-cell lining the blood vessels and represents an interface between blood and tissue. It acts as a selective permeability barrier, regulates coagulation and contributes to the behaviour of cells both in the circulation and in the vessel wall. Because of its location, one of the most important function of the endothelium is the regulation of the movement from the vascular to the extravascular space of water and solutes containing nutrients. Recent advances in our knowledge of the blood-brain barrier (BBB) have in part been made by studying the properties and function of cerebral endothelial cells (CECs) in vitro. After an era working with a fraction, enriched in cerebral microvessels by centrifugation, the next generation of in vitro BBB model systems was introduced, when the conditions for routinely culturing the endothelial cells were established. This review summarizes the results from this rapidly growing field. In addition to providing a better insight into the chemical composition of CECs, much has been learned from these studies about the characteristics of transport processes and cell-to-cell interactions during the last years. Astrocytes and neuronal elements contribute to the induction of BBB properties of CECs during ontogenesis and in tissue culture conditions. With the application of new technologies, the approach offers new means to investigation, applicable not only to biochemistry and physiology but also to the drug research, and may improve the transport of substances through the BBB. CECs grown on microporous cell culture inserts and co-cultured with astrocytes or treated by astrocyte-conditioned media proved to be excellent models for studying the direct effects of mediators and second messengers on the transendothelial permeability. The in vitro approach has been and should remain an excellent model of the BBB to help unravel the complex molecular interactions underlying and regulating the permeability of cerebral endothelium.

Animals↗
PubMed1996

Prenatal exposure to sodium bromide affects the postnatal growth and brain development.

Previous experiments suggest that bromide ions interfere with trophic interactions of neurons in intact adult rats and may modify reactive neuroplasticity during postnatal development. Here we report on bromide effects on normal development. Rat embryos were exposed to sodium bromide (NaBr) by providing an aqueous solution of 250 mg/% NaBr in the drinking water, ad libitum, to their dams. Controls received either tap water or saline (250 mg%NaCl) to drink. Application to dams was restricted to the 5th to 15th days of gestation. Measurements of bromide concentrations in samples of blood and brain homogenates revealed, however, that bromide transfer to embryos was not restricted to the treatment period. Because of delayed excretion dams provided the offspring with bromide via placenta and milk up to 10 days after birth, although at decreasing concentrations. Significant delays in postnatal development were observed in all bromide-treated animals. Permanent deficits were recorded for body weight, brain weight and the protein content of brain tissue. Additionally, there were some changes in brain structure, e.g. the laminar structure of the neocortex was modified. In contrast to developmental deficits, the size of olfactory glomeruli was consistently larger in bromide-treated rats during postnatal and glomeruli attained a mean diameter that was 30 percent larger than in controls at 3 months of age. Results suggest that pre- and perinatal exposure of rats to moderate concentrations of NaBr may interfere with postnatal development including that of brain. Since after complete excretion of bromide developmental deficits persist and show periods of partial compensation and decompensation, induction of these bromide effects is probably indirect. The exact mechanism of bromide action on developmental processes remains to be elucidated.

Age Factors↗
PubMed1995

Exposure of tumor necrosis factor-alpha to luminal membrane of bovine brain capillary endothelial cells cocultured with astrocytes induces a delayed increase of permeability and cytoplasmic stress fiber formation of actin.

Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood-brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1-hr exposure of recombinant human TNF-alpha (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelial flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P < 0.05) in sucrose permeation at 2-4 hr with the highest dose of TNF-alpha. On the other hand, at 16 hr after the 1-hr challenge with TNF-alpha (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F-actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF-alpha by a delayed increase of permeability and reorganization of actin filaments.

Actins↗
PubMed1995

Identification of the Ulex europaeus agglutinin-I-binding protein as a unique glycoform of the neural cell adhesion molecule in the olfactory sensory axons of adults rats.

Histochemical localization of two lectins, Ulex europaeus agglutinin-I (UEA-I) and Tetragonolobus purpureus (TPA), was studied in the olfactory bulb of adult rats. In contrast to TPA, UEA-I detected a fucosylated glycoprotein that is only present in the surface membranes of olfactory sensory cells including the whole course of their neurites up to the final arborization in glomeruli. Immunoblotting revealed that UEA-I binds specifically to a protein of 205 kDa, while TPA stains several other glycoproteins. Affinity chromatography with the use of a UEA-I column identified the 205 kDa protein as a glycoform of neural cell adhesion molecule (N-CAM), specific for the rat olfactory sensory nerves.

Agglutinins↗
PubMed1995

The role of cerebral microvessels in the elimination of histamine released during postasphyxial reperfusion in newborn piglets.

Histamine, released from intracerebral sources during hypoxic-ischemic conditions, may take part in the pathogenesis of neonatal brain injuries. In order to elucidate the possible role of cerebral microvessels in the elimination of histamine from the extracellular space, we determined the concentration of histamine using a modified radioenzymatic method in plasma taken from the internal jugular vein, in cerebrospinal fluid, and in capillary-rich fraction of cerebral microvessels prepared from cortex in 12 sham-operated piglets. Then, bilateral pneumothorax was induced in 20 piglets, samples were taken from the same compartments as from the controls before and during asphyxia, as well as 15 and 180 min thereafter, respectively. Plasma histamine level was significantly (P < 0.05) elevated in animals during hypoxic cardiovascular and metabolic failure (13.5 +/- 1.9 nM l-1) compared to value measured in the control group (2.2 +/- 0.5 nM l-1), preceding any detectable change of histamine concentration in cerebrospinal fluid (5.2 +/- 1.9 versus 3.8 +/- 1.1 nM l-1, respectively) or in cerebral microvessels (8.4 +/- 0.8 versus 7.1 +/- 0.6 pM (mg protein)-1). After resuscitation, histamine levels in plasma samples remained high during the early (15 min, 16.2 +/- 4.3 nM x l-1) and late (180 min, 15.3 +/- 2.9 nM l-1) reperfusion period. By contrast, histamine concentration was increased considerably (P < 0.05) in cerebrospinal fluid samples obtained 15 min (12.8 +/- 6.5 nM l-1), but not 180 min (5.2 +/- 1.9 nM l-1) after resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Carrier-mediated uptake and release of histamine by cultured rat cerebral endothelial cells.

The present study demonstrates that histamine could be taken up by and released from endothelial cells of brain capillaries. Incubation of cultured endothelial cells, with low (0.01-0.50 microM) concentrations of [3H]histamine, resulted in a rapid uptake of the amine. The uptake was saturable, Na(+)-dependent and yielded an apparent Km 0.3 +/- 0.02 microM and a Vmax 4.6 +/- 0.04 pmol/mg protein per min. After a 10-min incubation in a histamine-free medium, about 65% of [3H]histamine was released from the cells. Na(+)-deprivation and high K+, as well as the treatment of the cells with ouabain affected the release, resulting in significantly higher rates of the efflux. The ability of cerebral endothelial cells to take up histamine from both luminal and abluminal sides but to release it mainly luminally, may function as an important mechanism to protect the neural tissue from the harmful effects of this endogenous mediator of inflammation.

Animals↗
PubMed1995

Atrial natriuretic peptide (ANP) attenuates brain oedema accompanying experimental subarachnoid haemorrhage.

The effects of centrally administered atrial natriuretic peptide (ANP) on the brain water and electrolyte contents were investigated in a rodent subarachnoid haemorrhage (SAH) model. SAH caused statistically significant increases in the brain sodium and water contents, while the potassium content did not change significantly, indicating that the brain oedema could be classified as having a primarily vasogenic component. Two micrograms or 5 micrograms of rat ANP administered into the lateral ventricle at the time of SAH induction statistically significantly decreased the water and sodium accumulation measured 90 minutes following SAH. The same treatment did not inhibit development of brain oedema measured 3 hours following SAH. However, when 5 micrograms of ANP was administered intraventricularly at the time of SAH induction and also 90 minutes later, the brain oedema 3 hours following SAH was again reduced statistically significantly. These effects of ANP were found not to be mediated by primary changes in serum osmolality and electrolyte concentrations. The present results confirm that centrally administered ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation in SAH-induced brain oedema. The potentials of influencing the central neuro-endocrine system as a novel way of the treatment of brain oedema are discussed.

Animals↗
PubMed1995

Chloride is preferentially accumulated in a subpopulation of dendrites and periglomerular cells of the main olfactory bulb in adult rats.

GABA is predominantly an inhibitory transmitter. Mediated by GABAA receptors, GABA opens chloride channels, induces a passive flux of chloride ions, which is usually directed from extracellular to intracellular space, and hyperpolarizes postsynaptic neurons. Recent electrophysiological data suggested that GABA may also depolarize neurons and exert excitatory actions. However, it remained unclear whether excitatory GABA effects are based on reversed transmembrane chloride gradient due to modifications in extracellular or intracellular chloride concentrations. Here, the first histochemical evidence is provided for local redistribution of chloride in the CNS of healthy adult rats. Olfactory bulbs were examined using freeze substitution, silver trapping of chloride and intensification techniques at light and electron microscopic level. The chloride content of precipitates was evidenced by electron spectroscopic imaging using a CEM 902 (Zeiss) electron microscope. Chloride concentration was high in a subpopulation of some periglomerular cell bodies and isolated dendritic profiles, while it seemed to be very low in certain parts of the glomerular neuropil including intercellular clefts. Data suggest that reversed chloride gradients can be demonstrated by cytochemical methods, and may be responsible for excitatory GABA effects on selected periglomerular neurons and dendrites in the olfactory glomeruli. Conditions leading to chloride redistribution in the CNS of normal adult rats remain to be determined.

Animals↗
PubMed1995

Expression of protein kinase C family members in the cerebral endothelial cells.

The protein kinase C (PKC) family is composed of at least four conventional (alpha, beta I, beta II, and gamma) and several related novel (delta, epsilon, eta, and zeta) isoforms with different distribution and sensitivity to Ca2+ and phorbol esters. The enzyme is known to be present in cerebral endothelial cells. We have investigated the occurrence of seven isoforms (alpha, beta, gamma, delta, epsilon, eta, and zeta) by using reverse transcriptase-polymerase chain reaction in rat brain, in a freshly isolated brain microvessel fraction, in primary cultures of rat brain endothelial cells, in an immortalized rat brain endothelial cell line, and in aortic endothelial cell cultures. Brain tissue contained all seven investigated isoforms. A similar expression pattern was seen in freshly purified microvessels, but the PKC-gamma isoform could not be detected. Primary cultures of endothelial cells expressed PKC-alpha, -beta, -delta, -eta, and -epsilon isoenzymes, whereas the immortalized cell line expressed PKC-alpha, -delta, -epsilon, and -eta. The rat aortic endothelium contained only PKC-alpha and -delta isoforms. The variety of expression patterns of PKC family members in endothelial cells of different type may reflect differences in the functional responsiveness to environmental stimuli. Because PKC has been shown to be involved in the regulation of the blood-brain barrier permeability, the presence of different isoforms may confer a sophisticated intracellular regulatory mechanism to the brain endothelial cells.

Animals↗
PubMed1995

Penetration of small molecular weight substances through cultured bovine brain capillary endothelial cell monolayers: the early effects of cyclic adenosine 3',5'-monophosphate.

Second messengers, such as cyclic adenosine 3',5'-monophosphate (cAMP), have been shown to take part in the regulation of blood-brain barrier permeability. In the present study, elevation of cAMP levels decreased sucrose (mol. wt, 342) and inulin (mol. wt, 5000) permeability across monolayers of bovine brain capillary endothelial cells as early as 1 h after exposure. Since both tracers use predominantly a paracellular pathway, we assume that cAMP may increase the tightness of the tight junctions through protein phosphorylation.

Animals↗
PubMed1994

Treatment with ranitidine of ischemic brain edema.

Cerebral ischemia was produced by bilateral common carotid artery occlusion in female Sprague-Dawley rats. Ranitidine, a histamine H2 receptor blocking agent, given intraperitoneally 30 min prior to ischemia, exerted a dose-dependent protective effect on water accumulation and ion shifts in the brain (Na+, K+ and Ca2+). To decide whether ranitidine can prevent ischemia-induced brain edema when given in the postischemic period, ranitidine (10 mg/kg i.p.) was administered 1, 2, and 3 h respectively after the onset of cerebral ischemia. Early (1 h) postocclusion treatment was still able to attenuate the ischemia-induced water accumulation and maldistribution of ions in the brain tissue.

Analysis of Variance↗
PubMed1994

Insight into the regulation by second messenger molecules of the permeability of the blood-brain barrier.

Recent advances in our knowledge of the blood-brain barrier have in part been made by studying the properties and function of cerebral endothelial cells in vitro. After an era of working with a fraction, enriched in cerebral microvessels by centrifugation, the next generation of in vitro blood-brain barrier model systems was introduced, when the conditions for routinely culturing the endothelial cells were established. This review summarizes the results obtained mainly from this in vitro approach. Different elements of the intracellular signaling messenger systems have been detected in the course of our studies in the cerebral endothelial cells. It has been shown that the synthesizing enzymes of and substrate proteins for the second messenger molecules are present in the cerebral endothelial cells, and their activity and/or amount can change in pathological circumstances, i.e., during the formation of brain oedema. Pharmacological treatments interfering with the second messenger systems proved to be effective in the prevention of brain oedema formation.

Animals↗
PubMed1994

In situ modification of the phospholipid environment of native rabbit sarcoplasmic reticulum membranes.

A water soluble hydrogenation catalyst (palladium di(sodium alizarine monosulphonate)) in a deuterium-containing environment has been used for the in situ insertion of deuterium atoms into the fatty acyl chains of biological membranes. The thermotropic response of the stretching vibrations of the formed C-D bonds, as detected by Fourier transform IR spectroscopy, was used as a selective probe of biological membrane structure. Partial deuteration of unsaturated fatty acyl chains coupled with IR detection potentially provides a means for detecting specific biological roles of particular lipid classes. In the current study of sarcoplasmic reticulum membranes and purified phospholipid/CaATPase vesicles, it is also shown that vC-D monitors change at particular membrane locations which may remain undetected through the CH2 symmetric stretching frequency, a widely used IR spectral parameter. The latter reflects the average environment of the acyl chains. The approach described here may be suitable for wide applications to the study of biomembranes.

Animals↗
PubMed1994

Platelet membrane fluidity and plasma malondialdehyde levels in Alzheimer's demented patients with and without family history of dementia.

Platelet membrane fluidity (PMF) was measured with three different fluorescent probes, 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH), 3-(p-phenyl-1,3,5-hexatrienyl)phenyl-propionic acid (DPH-PA), which labeled different parts of the bilayer (the hydrophobic core and the positively and negatively charged regions, respectively) in Alzheimer's disease (AD) patients with and without a family history of dementia, and in a control group. In support of earlier findings in the literature, significantly increased PMF was found by the application of DPH in both groups with AD. The use of the fluorescence probe TMA-DPH, however, revealed no differences between the groups. In contrast, significant rigidification was observed with DPH-PA, but only in the AD group with a positive family history of dementia. The plasma malondialdehyde levels appeared to be similar in each group. Our findings are discussed in light of the controversies regarding the value of PMF measurements in AD.

Aged↗
PubMed1994

The role of histamine in brain oedema formation.

The effects of histamine on the cerebral endothelial cells were studied. To determine if the extent of brain oedema formation could be reduced with histamine receptor antagonists, mepyramine (H1-receptor blocker), metiamide, cimetidine and ranitidine (H2-receptor antagonists) were administered at a dose of 5 mg/kg body weight 4, 2 and 0 h before the onset of experimental pneumothorax induced in newborn piglets. Mepyramine and ranitidine given 2 h before the induction of EBP prevented the accumulation of water, sodium and albumin in samples taken from the parietal cortex. In other experiments, carried out on Sprague-Dawley rats of CFY strain after permanent bilateral common carotid ligation (BCCL), the accumulation of water and sodium in the ischemic brain tissue could also be prevented in a dose dependent manner by intraperitoneal injections of ranitidine given 30 min before the surgery. Taken together, these results provide pharmacological evidence for the involvement of histamine receptors in the pathogenesis of brain oedema. Consequently, the use of histamine receptor blockers both in the prevention and in the treatment of brain oedema can be recommended.

Animals↗