bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trafficking of PLP/DM20 and cAMP signaling in immortalized jimpy oligodendrocytes
Authors: Ghandour M. Said , Feutz Anne‐Catherine , Jalabi Walid , Taleb Omar , Bessert Denise , Cypher Maria , Carlock Leon , Skoff Robert P. 
Published: November 2002

AbstractThe synthesis, transport, and insertion of jimpy proteolipid protein and DM20 were studied in normal (158N) and jimpy (158JP) immortalized oligodendrocyte lines. Four different expression vectors encoding fusion proteins composed of native PLP and DM20 or jimpy PLP or DM20 were linked to enhanced green fluorescent protein (EGFP). All four transfected fusion proteins had similar distributions in the cell bodies and processes of the two cell types. Both normal and jimpy PLP‐EGFP and DM20‐EGFP were detected in both cell lines as far as 200 μm from the cell body, indicating synthesis and transport of mutated PLP and DM20 toward the plasma membrane. Immunocytochemistry of fixed normal and jimpy cells with the O10 antibody, which recognizes a conformationally sensitive PLP/DM20 epitope, confirmed that normal and jimpy PLP and DM20 were transported to the plasma membrane. Live staining of normal and jimpy cells transiently transfected with the native PLP showed positive staining, indicating PLP was correctly inserted into the membrane of both normal and jimpy oligodendrocytes. However, live staining of normal and jimpy cells transiently transfected with jimpy PLP showed no positive staining, indicating the mutated protein is abnormally inserted into the plasma membrane. Electrophysiological recordings of the resting membrane potential measured in the whole cell mode of the patch‐clamp technique showed the absence of a developmentally regulated negative shift in the membrane potential in jimpy cells compared to normal native or immortalized oligodendrocytes. Treatment of 158N cells and native oligodendrocytes with dibutyryl cAMP (dbcAMP) caused morphological and biochemical differentiation, but failed to do so in 158JP cells, suggesting an abnormal signaling pathway in jimpy. The defect in cAMP signaling in jimpy oligodendrocytes was associated with the suppression of increase in mRNA level of the inducible cAMP early repressor (ICER). When the jimpy oligodendrocyte line was transfected with normal PLP or DM20 and exposed to dbcAMP, the cells failed to differentiate. This finding suggests that improper insertion of jimpy protein into the plasma membrane alters the membrane in such a way that certain signaling pathways are permanently altered. The abnormal insertion of jimpy PLP/DM20 into the plasma membrane may be the basis for the lack of cell signaling and abnormal resting potential in jimpy oligodendrocytes. GLIA 40:300–311, 2002. © 2002 Wiley‐Liss, Inc.
Catecholamine‐induced oligodendrocyte cell death in culture is developmentally regulated and involves free radical generation and differential activation of caspase‐3
Authors: Khorchid Amani , Fragoso Gabriela , Shore Gordon , Almazan Guillermina 
Published: November 2002

AbstractOligodendrocyte cultures were used to study the toxic effects of catecholamines. Our results showed that catecholamine‐induced toxicity was dependent on the dose of dopamine or norepinephrine used and on the developmental stage of the cultures, with oligodendrocyte progenitors being more vulnerable. A role for oxidative stress and apoptosis on the mechanism of action of catecholamines on oligodendrocyte cell death was next assessed. Catecholamines caused a reduction in intracellular glutathione levels, an accumulation in reactive oxygen species and in heme oxygenase‐1, the 32 kDa stress‐induced protein. All these changes were prevented by N‐acetyl‐L‐cysteine, a thiocompound with antioxidant activity and a precursor of glutathione, and were more pronounced in progenitors than mature cells, which could contribute to their higher susceptibility. Apoptotic cell death, as assessed by activation of caspase‐9 and –3 and cleavage of poly(ADP‐ribose) polymerase (a substrate of caspase‐3), was only observed in oligodendrocyte progenitors. Pretreatment with zVAD, a general caspase inhibitor, prevented activation of caspase‐9 and ‐3, DNA fragmentation, and decreased progenitors cell death. Furthermore, the expression levels of procaspase‐3 and the ratio of the proapoptotic protein bax to antiapoptotic protein bcl‐xl were several folds higher in immature than mature oligodendrocytes. Taken together, these results strongly suggest that the catecholamine‐induced cytotoxicity in oligodendrocytes is developmentally regulated, mediated by oxidative stress, and have characteristics of apoptosis in progenitor cells. GLIA 40:283–299, 2002. © 2002 Wiley‐Liss, Inc.
Nitric oxide induces rapid, calcium‐dependent release of vesicular glutamate and ATP from cultured rat astrocytes
Authors: Bal‐Price Anna , Moneer Zahid , Brown Guy C. 
Published: November 2002

AbstractNitric oxide (NO; 1 μM) or an NO donor (500 μM diethylenetriamine‐nitric oxide, DETA‐NONOate) caused rapid glutamate and ATP release from cultured rat cortical astrocytes. NO‐induced glutamate release was prevented by calcium chelators (EGTA or BAPTA‐AM) and an inhibitor of vesicular exocytosis (botulinum neurotoxin C, BoTx‐C), but not by a glutamate transport inhibitor, L‐trans‐pyrrolidine‐2,4‐dicarboxylate (t‐PDC), a cyclooxygenase inhibitor (indomethacin), or an inhibitor of soluble guanylate cyclase 1H‐[1,2,4]oxadiazolo‐[4,3‐a]quinoxalin‐1‐one (ODQ), and was not induced by mitochondrial respiratory inhibitors (myxothiazol or azide). Similarly to glutamate, NO‐induced ATP release was also completely blocked by BAPTA‐AM and BoTx‐C, suggesting again a vesicular, calcium‐dependent mechanism of release. Addition of DETA‐NONOate (500 μM) to fura‐2–loaded astrocytes induced a rapid, transient increase in intracellular calcium levels followed by a lower, sustained level of calcium entry. The latter was blocked by gadolinium (1 μM), an inhibitor of capacitative Ca2+ entry. Thus, NO appears to cause rapid exocytosis of vesicular glutamate and ATP from astrocytes by raising intracellular calcium levels. Astrocytes activated by lipopolysaccharide/endotoxin and interferon‐γ to express inducible NO synthase (iNOS) maintained substantially higher extracellular glutamate levels than nonactivated cells or activated cells treated with an iNOS inhibitor (1400W), but the rate of glutamate uptake by these cells was similar. This suggests that NO from inflammatory‐activated astrocytes causes release of astrocytic glutamate. NO‐induced release of astrocytic glutamate and ATP may be important in physiological or pathological communication between astrocytes and neurons. GLIA 40:312–323, 2002. © 2002 Wiley‐Liss, Inc.
Ammonia‐induced heme oxygenase‐1 expression in cultured rat astrocytes and rat brain in vivo
Authors: Warskulat Ulrich , Görg Boris , Bidmon Hans‐J. , Müller Hans Werner , Schliess Freimut , Häussinger Dieter 
Published: November 2002

AbstractAmmonia is a key factor in the pathogenesis of hepatic encephalopathy (HE), which is a major complication in acute and chronic liver failure and other hyperammonemic states. The molecular mechanisms underlying ammonia neurotoxicity and the functional consequences of ammonia on gene expression in astrocytes are incompletely understood. Using cDNA array hybridization technique we identified ammonia as a trigger of heme oxygenase‐1 (HO‐1) mRNA levels in cultured rat astrocytes. As shown by Northern and Western blot analysis, HO‐1 mRNA levels were upregulated by ammonia (0.1–5 mmol/L) after 24 h and protein expression after 72 h in astrocytes. These ammonia effects on HO‐1 are probably triggered to a minor extent by ammonia‐induced glutamine synthesis or by astrocyte swelling, because HO‐1 expression was not inhibited by the glutamine synthetase inhibitor methionine sulfoximine (which abrogated ammonia‐induced cell swelling in cultured astrocytes), and ammonia‐induced HO‐1 expression could only partly be mimicked by hypoosmotic astrocyte swelling. Hypoosmotic (205 mOsm/L) exposure of astrocytes led even to a decrease in HO‐1 mRNA levels within 4 h, whereas hyperosmotic (405 mOsm/L) exposure increased HO‐1 mRNA expression. After 24 h, hypoosmolarity slightly raised HO‐1 mRNA expression. Taurine and melatonin diminished ammonia‐induced HO‐1 mRNA or protein expression, whereas other antioxidants (dimethylthiourea, butylated hydroxytoluene, N‐acetylcysteine, and reduced glutathione) increased HO‐1 mRNA levels under ammonia‐free conditions. An in vivo relevance is suggested by the finding that increased HO‐1 expression occurs in the brain cortex from acutely ammonia‐intoxicated rats. It is concluded that ammonia‐induced HO‐1 expression may contribute to cerebral hyperemia in hyperammonic states. GLIA 40:324–336, 2002. © 2002 Wiley‐Liss, Inc.
The tetraspanin protein, CD9, is expressed by progenitor cells committed to oligodendrogenesis and is linked to β1 integrin, CD81, and Tspan‐2
Authors: Terada Nobuo , Baracskay Karen , Kinter Mike , Melrose Shona , Brophy Peter J. , Boucheix Claude , Bjartmar Carl , Kidd Grahame , Trapp Bruce D. 
Published: November 2002

AbstractPrevious studies identified the tetraspanin protein CD9 in myelinating oligodendrocytes. The present report extends these observations by identifying CD9 in a subpopulation of oligodendrocyte progenitor cells (OPCs) and in premyelinating oligodendrocytes in rodents. NG2‐positive cells expressed CD9 in a temporal and spatial pattern during development that was consistent with CD9 expression in OPCs just prior to their differentiation into premyelinating oligodendrocytes. NG2‐positive cells in mature brains were CD9‐negative. CD9 expression during oligodendrocyte development in vitro supported this hypothesis, as all CD9‐positive cells became O4‐positive when switched to oligodendrocyte differentiating media. CD9 immunoreactivity was enriched in myelinating oligodendrocytes and their processes, and the outer aspects of myelin internodes. Immunoprecipitation of CD9 from postnatal rat cerebrum coprecipitated β1 integrin, CD81, and Tspan‐2, another tetraspanin protein recently identified in oligodendrocytes. Following surface biotinylation of oligodendrocytes in vitro, biotinylated β1 integrin was identified in a CD9 immunoprecipitate. These data support a molecular link between surface integrins and a CD9, Tspan‐2 molecular web during the differentiation of oligodendrocytes. Oligodendrocyte production and myelination appears to be normal in CD9‐deficient mice. These data support the hypothesis that CD9 helps form the tetraspanin web beneath the plasma membranes of progenitor cells committed to oligodendrogenesis, but that CD9 is not essential for oligodendrogenesis and myelination. GLIA 40:350–359, 2002. © 2002 Wiley‐Liss, Inc.
Selective inflammatory stimulations enhance release of microglial response factor (MRF)‐1 from cultured microglia
Authors: Tanaka Shuuitsu , Koike Tatsuro 
Published: November 2002

AbstractThe mrf‐1 gene has been isolated from microglia exposed to cultured cerebellar granule neurons undergoing apoptosis. We have shown that mrf‐1 is upregulated in response to neuronal death and degeneration both in vitro and in vivo. However, the exact role of MRF‐1 remains unknown. Here we show that MRF‐1 is released from cultured rat microglia, and its release is greatly enhanced under inflammatory conditions. When microglia were treated with ATP, the amount of MRF‐1 that was released increased 10‐fold compared to the basal level of release. Enhanced MRF‐1 release was induced within 10 min and peaked within 1 h; after ∼ 4 h, the MRF‐1 release had returned to normal. MRF‐1 release was stimulated by 2‐methyl‐thio‐ATP (five‐fold) and a P2X7 selective agonist, 2′‐ and 3′‐O‐(4‐benzoylbenzoyl)‐ATP (ten‐fold). Moreover, the ATP‐stimulated MRF‐1 release was inhibited by a P2X7 selective antagonist, oxidized ATP (oATP), and also under a Ca2+‐free condition. These results indicate that the effects of ATP are dependent on Ca2+ influx through P2X7 receptors. MRF‐1 release was enhanced by Ca2+‐ionophore A23187 (sixfold), thapsigargin (threefold); however, it was not enhanced by glutamate or lipopolysaccharide. Moreover, a platelet‐activating factor enhanced microglial MRF‐1 release in a dose‐dependent manner. We also showed that a conditioned medium from cerebellar granule neurons undergoing apoptosis markedly increased MRF‐1 release from microglia; that effect was significantly inhibited by oATP. These results indicate that selective inflammatory stimulations, including ATP and PAF, enhance MRF‐1 release from microglia through a Ca2+‐dependent mechanism and suggest that MRF‐1 may play a role in cell‐cell interactions under inflammatory conditions. GLIA 40:360–371, 2002. © 2002 Wiley‐Liss, Inc.
cAMP‐dependent reorganization of the Cajal bodies and splicing machinery in cultured Schwann cells
Authors: Fernandez Rosario , Pena Emma , Navascues Joaquin , Casafont Iñigo , Lafarga Miguel , Berciano Maria T. 
Published: November 2002

AbstractIt is well established that forskolin‐induced elevation of cAMP results in activation of DNA synthesis in Schwann cell cultures. This promitotic response is partially mediated by the Cdk2, which is required for the transition from the G1 to the S phase of the cell cycle. In the present study, we analyze the effects of cAMP elevation in cultured Schwann cells on the transcriptional activity and on the organization of two nuclear compartments involved in pre‐mRNA processing: Cajal bodies (CBs) and splicing factor compartments. Our immunofluorescence and quantitative studies show that forskolin treatment induces a 5.6‐fold increase in the proportion of S phase Schwann cells, detected by a short pulse (20 min) of BrdU incorporation. This increase in DNA synthesis correlates with an activation of global transcription, as is indicated by the higher nuclear incorporation of BrU in nascent RNA. Forskolin treatment significantly increases the percentage of Schwann cells containing typical CBs, which concentrate spliceosomal snRNPs and the survival motor neuron (SMN) protein. This increase in the number of CBs closely correlates with the activation of transcription. Moreover, the occurrence of CBs is significantly higher in BrdU (+) cells than in BrdU (−) cells, indicating that entry in the S phase promotes the formation of CBs. During the S phase, Schwann cell nuclei display higher Cdk2 nuclear staining and concentrate this kinase in CBs. Forskolin also induces a redistribution of the pre‐mRNA splicing factors in Schwann cells. Primary cultures of Schwann cells provide an excellent physiological model to demonstrate that the assembly of CBs is a transcription‐ and replication‐dependent cellular event. Moreover, the S phase accumulation of Cdk2 observed in Schwann cells supports a functional link between CBs and DNA replication, which is mediated by the possible participation of CBs in the regulatory control of histone gene expression. GLIA 40:378–388, 2002. © 2002 Wiley‐Liss, Inc.
Structure of the tarsi in some stenus species (coleoptera, staphylinidae): External morphology, ultrastructure, and tarsal secretion
Authors: Betz Oliver 
Published: November 2002

AbstractSEM studies show that the differentiation among Stenus species with respect to the formation of the tarsi (wide bilobed vs. slender tarsomeres) takes place with a considerable augmentation of tarsal ventral setae in wide bilobed tarsomeres. The structural diversity of ventral tarsal setae among and within species is discussed with respect to 1) their different roles as mechanosensilla and tenent setae, respectively, and 2) the different selection pressures in terms of adhesive requirements along the longitudinal tarsus axis. The tarsi are provided with four groups of tarsal mechanosensilla, comprising hair and bristle sensilla, campaniform sensilla, and scolopidia. The tarsus wall is supported by an epidermis, which forms three different types of glands pouring their secretion via different exit paths onto the outer cuticle. The organization and ultrastructure of each of these glands is described. Only one (unicellular) gland is directly associated with the ventral tenent setae and is thus considered to form the main part of the adhesive secretion. The beetles appear to release the tarsal secretion through mediation of the tenent setae, which contains a lipid and a proteinaceous fraction. I propose that the secretion is discharged to the outside via a system of very fine pore canals in the wall of the setal shaft. Gas chromatography and infrared spectroscopy revealed that the lipid fraction of the secretion is a mixture of unsaturated fatty acid glycerides and aliphatic hydrocarbons whose spectra are similar to those of extractions of the superficial lipid coating of the body surface. J. Morphol. 255:24–43, 2003. © 2002 Wiley‐Liss, Inc.
Development of the supraorbital and mandibular lateral line canals in the cichlid, archocentrus nigrofasciatus
Authors: Tarby Melissa L. , Webb Jacqueline F. 
Published: November 2002

AbstractThe development of two of the cranial lateral line canals is described in the cichlid, Archocentrus nigrofasciatus. Four stages of canal morphogenesis are defined based on histological analysis of the supraorbital and mandibular canals. “Canal enclosure” and “canal ossification” are defined as two discrete stages in lateral line canal development, which differ in duration, an observation that has interesting implications for the ontogeny of lateral line function. Canal diameter in the vicinity of individual neuromasts begins to increase before ossification of the canal roof in each canal segment; this increase in canal diameter is accompanied by an increase in canal neuromast size. The mandibular canal generally develops later than the supraorbital canal in this species, but in both of these canals development of the different canal segments contained within a single dermal bone is asynchronous. These observations suggest that a dynamic process requiring integration and interaction among different tissues, in both space and time, underlies the development of the cranial lateral line canal system. The supraorbital and mandibular canals appear to demonstrate a “one‐component” pattern of development in Archocentrus nigrofasciatus, where the walls of each canal segment grow up from the underlying dermal bone and then fuse to form the bony canal roof. This is contrary to numerous published reports that describe a “two‐component” pattern of development in teleosts where the bony canal ossifies separately and then fuses with an underlying dermal bone. A survey of the literature in which lateral line canal development is described using histological analysis suggests that the occurrence of two different patterns of canal morphogenesis (“one‐component” and “two‐component”) may be due to phylogenetic variation in the pattern of the development of the lateral line canals. J. Morphol. 255:44–57, 2003. © 2002 Wiley‐Liss, Inc.
Complex genital structures indicate cryptic female choice in a haplogyne spider (arachnida, araneae, oonopidae, gamasomorphinae)
Authors: Burger Matthias , Nentwig Wolfgang , Kropf Christian 
Published: November 2002

AbstractFemale genital structures with their allied muscles of the haplogyne spider Opopaea fosuma are described. A functional explanation of this system is given, which indicates that cryptic female choice may occur in these spiders: the anterior wall of their spermatheca is strongly sclerotized and possesses a cone‐shaped hole in its upper part. A transverse sclerite that serves as muscle attachment bears a nail‐like structure and lies in a chitinized area of the anterior wall of the uterus externus. Muscle contraction presses this nail into the hole of the spermatheca. In this way, the uterus externus gets both locked and fixed. Furthermore, as this occurs the copulatory orifice is enlarged and the resulting suction probably leads to previously deposited sperm being drawn from the spermatheca and dumped. This is a common mechanism used by females to influence a male's chances of fathering their offspring in a process known as cryptic female choice. J. Morphol. 255:80–93, 2003. © 2002 Wiley‐Liss, Inc.
Cranial osteology of the andean lizardstenocercus guentheri(Squamata: Tropiduridae) and its postembryonic development
Authors: Torres‐Carvajal Omar 
Published: November 2002

AbstractIn spite of the great diversity of iguanian lizards, detailed descriptions of their osteocrania and postembryonic development are rare. Herein, the adult cranial osteology of the tropidurid lizardStenocercus guentheriand its postembryonic development are described based on cleared and double‐stained and dry skeletal specimens from a single Ecuadorian population. The amphikinetic skull ofS. guentheriis short and elevated and bears teeth on the premaxilla, maxillae, and pterygoids. Mandibular teeth are present on the dentaries. Ossification of the articular from Meckel's cartilage and growth of the parietal (ossification and investment of the frontoparietal fontanelle) are the most significant ontogenetic changes of the splanchnocranium and dermatocranium, respectively. The ossification of the cartilage separating the bones of the braincase is the most relevant postembryonic ontogenetic event of the neurocranium. The number of teeth does not vary ontogenetically and replacement teeth are present throughout postembryonic life. This study includes a list of the osteocranial characters ofStenocercusthat have been used in systematic studies, as well as a discussion of functional morphology and kinesis. J. Morphol. 255:94–113, 2003. © 2002 Wiley‐Liss, Inc.
Developmental origin of the frontoparietal bone in bombina variegata (anura: discoglossidae)
Authors: Čihák Radomír , Královec Karel , Roček Zbyněk 
Published: November 2002

AbstractDevelopment of the frontoparietal bone in the European yellow‐bellied toad, Bombina variegata, was followed on the basis of histological analysis of transverse serial sections through the larval skulls to recognize early stages of ossification represented by osteoid (uncalcified bone matrix) and on cleared and stained specimens to investigate more advanced stages. Ossification of the frontal begins as three tiny areas of osteoid (F1, F2, F3) adjoining the dorsal surface of the orbital cartilage, which are separated by areas without osteoid. F3 is the largest (most advanced). Prior to calcification, F3 extends to fuse with F2 and then with F1, but it does not expand over the prootic fissure posteriorly. As calcification begins the strip of bone is joined posteromedially by F4. Only then does a single ossification center corresponding to the parietal arise on the anterodorsal surface of the otic capsule. This ossification sequence corresponds to those observed in the Actinopterygii and in caudate amphibians. J. Morphol. 255:122–129, 2003. © 2002 Wiley‐Liss, Inc.
Application service providers (ASPs): new impetus for transformational change
Authors: Kakabadse Andrew , Kakabadse Nada 
Published: November 2002

AbstractApplication service providers (ASPs) are a business phenomenon of the Internet age. The ASP concept offers companies the rewards of best‐in‐class application functionality for a fixed monthly cost and easy usage scalability, thus liberating organizations from technological complexities. In exploring the effectiveness of the ASP model, this paper examines the development of ASPs and also reports the results of a UK study, 178 ASP service purchasers and providers, highlighting the nature and offerings of service providers and the levels of satisfaction with ASP services. It is argued that the ASPs' potential to induce transformational change in terms of business processes and thus on the total enterprise is extensive. Also, by highlighting concerns with current ASP services, the paper concludes on an optimistic note emphasizing a favourable outlook for ASPs in the future. Copyright © 2002 John Wiley & Sons, Ltd.