bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transforming growth factor beta expression in reactive spinal cord microglia and meningeal inflammatory cells during experimental allergic neuritis
Authors: Kiefer R. , Gold R. , Gehrmann J. , Lindholm D. , Wekerle H. , Kreutzberg G. W. 
Published: January 2005

AbstractExperimental allergic neurities (EAN), an inflammatory demyelinating disorder of the peripheral nervous system, is preceded and accompanied by a massive microglial reaction in the spinal cord which occurs in the absence of inflammatory cells infiltrating the cord parenchyma. Since transforming growth factor beta (TGF‐β) has been shown to play a beneficial role in experimental autoimmune disease and might be involved in the regulation of glial activity, we have investigated the expression of TGF‐β in EAN spinal cord and nerve root tissue. Adoptive transfer EAN was induced by the injection of neurotogenic T‐cells specific for the P2 myelin protein. In normal spinal cord tissue, both TGF‐β1 and TGF‐β3 mRNA were constitutively expressed at low levels. Already 3 days following injection of P2‐specific T‐cells, TGF‐β1 mRNA levels began to increase, peaked at day 6 at levels about tenfold above normal, and thereafter declined. TGF‐β3 was induced even earlier with a sharp rise at day 3 and a peak fourfold above normal at day 4. In situ hybridization for TGF‐β1 performed on spinal cord sections 6 days after injection of cells localized TGF‐β1 mRNA to many nonneuronal cells with the typical morphology of microglia. In addition, TGF‐β1 mRNA was observed in the meninges, and massive accumulation of signal was seen over inflammatory cells infiltrating the nerve roots. Our data indicate that TGF‐β1 and ‐β3 are involved in regulating the glial response in EAN and that activated microglial cells might control their own activity state by expressing TGF‐β1. The expression of TGF‐β1 by infiltrating inflammatory cells in the nerve roots might represent an important endogenous mechanism to limit the extent of inflammation. © 1993 Wiley‐Liss, Inc.
Selective expression of foreign genes in glioma cells: Use of the mouse myelin basic protein gene promoter to direct toxic gene expression
Authors: Miyao Y. , Shimizu K. , Moriuchi S. , Yamada M. , Nakahira K. , Nakajima K. , Nakao J. , Kuriyama S. , Tsujii T. , Mikoshiba K. , Hayakawa T. , Ikenaka K. 
Published: January 2005

AbstractWe have previously demonstrated that retrovirusmediated genes were transferred to mouse glioma cells in a meningeal gliomatosis model (Yamada et al.: Japanese Journal of Cancer Research 83:1244–1247, 1992). This retrovirus vector contains the Escherichia coli. β‐galactosidase (β‐gal) gene as a marker for intergration of the lacZ gene, which is controlled by the SV40 early promoter. We investigated whether lacZ genes could be specifically controlled in mouse glioma cells by glial‐specific promoters, including the 2.5 kb 5′ flanking region of the mouse glial fibrillary acidic protein (GFAP) gene, the 1.3 kb 5′ flanking region of the myelin basic protein (MBP) gene, and the 1.5 kb 5′ flanking region of the myelin proteolipid protein (PLP) gene. Psi‐2 packaging cells were transfected with each retrovirus vector (GFAP promoter‐, MBP promoter‐, and PLP promoter‐lacZ) and the infectious virus particles were recovered from the supernatants. Blue staining for β‐gal was detected in various fibroblast, myeloma, and glioma cell lines transduced with the retrovirus BAAG vector. On the other hand, blue staining was only detected in glioma cells after transduction with the lacZ gene‐bearing retrovirus controlled by glial‐specific promoters. The strongest promoter activity was detected after transduction with the retrovirus in which the MBP promoter controlled the lacZ gene. Mouse glioma cells transduced with retrovirus containing the MBP promoter directing the herpes simplex virus type 1 thymidine kinase (HTK) gene wre extremely sensitive to ganciclovir, while the parental cells and cells transduced with retrovirus containing the lacZ gene were not sensitive to ganciclovir. Furthermore, none of the nonglioma cells tested was sensitive to ganciclovir, even when transduced with the MBP promoter‐HTK gene‐containing retrovirus. In conclusion, retrovirus targeted gene therapy of malignant glioma may be applicable with a low risk of side effects such as bone marrow suppression, in constrast to chemotherapy or the use of retroviruses bearing toxic genes controlled by nonspecific promoters. © 1993 Wiley‐Liss, Inc.
Cranin interacts specifically with the sulfatide‐binding domain of laminin
Authors: Smalheiser N. R. 
Published: January 2005

AbstractCranin is a 120 kDa integral membrane glycoprotein which binds laminin under conditions of physiologic ionic strength in a calcium‐dependent manner. Here, binding of cranin to laminin has been characterized using both ligand‐blotting assays and laminin affinity bead assays. Binding was specifically inhibited by anti‐laminin antibodies against the A chain terminal domain G, but not by several other region‐specific antibodies. Dextran sulfate, fucoidin, and sulfatide were potent inhibitors of binding (50% inhibition at 0.03, 0.5, and 1.7 μg/ml, respectively); heparin was a weaker inhibitor (50% inhibition ∼5 μg/ml), and mannan and chondroitin sulfate were not inhibitory at 100 μ/ml. Binding was not inhibited by lactose or the A chain peptide PA22‐2. The mobility of the broad, fuzzy cranin band was shifted after digestion with neuraminidase, N‐glycanase, and O‐glycanase, though none of these treatments decreased band heterogeneity nor destroyed the ability to bind laminin. Cranin bound to Jacalin lectin, which recognizes the Galβ1‐3GalNAc linkage expressed in certain classes of mucins. These findings indicate that cranin binds at or near the high affinity sulfatide‐binding site previously mapped to the E3 domain of laminin, which is known to exhibit bioactivity for neural cells. In view of the extremely low abundance of cranin in brain membranes (∼0.005%), its avid laminin‐binding activity is remarkable, and strongly suggests that cranin may play a physiologic role in regulating specific neural cell interactions. © 1993 Wiley‐Liss, Inc.
K252a potentiates epidermal growth factor‐induced differentiation of PC12 cells
Authors: Wu C.‐F. , Zhang M. , Howard B. D. 
Published: January 2005

AbstractEpidermal growth factor (EFG) induced short neurites in two different strains of PC12 cells. The length of the EGF‐induced neurites was markedly increased in the presence of the protein kinase inhibitor K252a, which is known to inhibit differentiation induced by nerve growth factor (NGF). EGF‐induced differentiation of PC12 required RNA synthesis and activity of the ras proto‐oncogene product. EGF increased the levels of three neurofilament proteins and the mRNA level of two late response genes (SCG10 and 63) known to be induced by NGF. Together, EGF and K252a caused a greater increase in these mRNAs than did either agent alone. K252a did not alter the extent of EGF‐induced autophosphorylation of the EGF receptor, but it did decrease the extent of receptor phosphorylation in the absence of added EGF. Thus, the ability of the EGF receptor to trigger neuronal differentiation may depend on the state of its phosphorylation at serine and/or threonine residues. Two other strains of PC12 did not extend neurites when exposed to EGF, even when K252a was also present. Thus the differentiating effect of EGF on PC12 is PC12 strain‐specific. © 1993 Wiley‐Liss, Inc.
Immunolocalization of proteolipid protein peptide 103–116 in myelin
Authors: Sobel R. A. , Greer J. M. , Isaac J. , Fondren G. , Lees M. B. 
Published: January 2005

AbstractDetermination of the topographic orientation of proteolipid protein (PLP) within myelin is part of an overall understanding of the functions of PLP and the roles of its multiple domains in diseases that primarily affect central nervous system (CNS) myelin. As part of an analysis of PLP orientation, two mouse monoclonal antibodies (mAb) and a rabbit antiserum against a synthetic peptide corresponding to PLP residues 103–116 (YKTTICGKGLSATV) were tested for their reactivity on compact CNS myelin. By ELISA, the antibodies react with intact PLP and PLP residues 103–116, but not with other PLP peptides. Ultrathin cryosections of adult rat optic nerve were immunostained and antibody binding was localized using appropriate second antibodies coupled to 1 nm gold particles that were visualized by silver enhancement. Localization of the particles on the major or intermediate dense lines was determined by three in dependent observers. Using the PLP peptide mAb and the polyclonal antibody, we demonstrated that ≥71% of the particles were localized on the major dense line. At least 66% of particles directed against myelin basic protein, which is known to occur on the major dense line, were also found in that location. These semiquantitative morphologic observations suggest that PLP residues 103–116 occur on the cytoplasmic face of the myelin membrane. © 1994 Wiley‐Liss, Inc.
Postnatal decrease of acetate concentration in rat cerebellum
Authors: Martin M. , Merele M. , Labouesse J. , Canioni P. 
Published: January 2005

AbstractWe examined the evolution of 1H‐NMR detectable metabolites in rat cerebellum fro the postnatal day 1–25, a period associated with intense metabolic changes as well as physiological and morphological modifications. The unexpected result reported here is the existence of a high concentration of acetate in neonatal rat cerebellum, progressively decreasing with age and maturation. In contrast, the cerebellum content of various metabolites such as N‐acetyl‐L‐as‐partate (NAA), glutamate, and aspartate increases from the first day onward. © 1994 Wiley‐Liss, Inc.
In vitro and in vivo characterisation of glial cells immortalised with a temperature sensitive SV40 T antigen‐containing retrovirus
Authors: Jung M. , Crang A. J. , Blackemore W. F. , Hoppe D. , Kettenmann H. , Trotter J. 
Published: January 2005

AbstractAn oncogene‐carrying repiication‐defective retrovirus was used to establish immortalised lines of murine glial cells. Primary cultures of early postnatal cerebellar cells were infected with a retrovirus based on the Murine Moloney Leukemia Virus containing a temperature‐sensitive mutant of the Simian Virus 40 large T antigen (SV40 T) oncogene and a gene coding for resistance to the antibiotic G418. Infected cells were selected in G418 and after several in vitro passages cells expressing the O4 antigen were established as a cell line. At a later time point O4‐positive single‐cell clones were established. Two different types of clones were obtained: (1) “plastic” clones consisting of cells which initially had a morphological and antigenic phenotype of young glial precursor cells but which gradually lost these features, and (2) “stable” cell clones including a clone with the immunological and electrophysiological characteristics of Schwann cells. Culture of the latter cells in the presence of 1 mM dibutyryl cyclic adenosine monophosphate for a period of at least 10 days induced a change in shape and a shift in antigen expression towards a more “diferentiated” maturation stage. When the SV40 T O4‐positive immortalised cell line isolated on the cell sorter was transplanted into demyelinated lesions in adult rats, cells were observed ensheathing axons and forming limited amounts of PNS‐type myelin.Glial cells immortalised with a temperature‐sensitive mutant of the SV40 T oncogene thus retain many physiological properties of their primary culture counterparts and can be induced to undergo limited differentiation in vitro and in vivo. These cell lines, which represent immature CNS glia or Schwann cells, are providing useful tools for investigating the role of cell surface antigens involved in neuron‐glial interactions. © 1994 Wiley‐Liss, Inc.
Cholinergic markers are expressed in developing and mature neurons of chick dorsal root ganglia
Authors: Tata A. M. , Plateroti M. , Cibati M. , Biagioni S. , Augusti‐Tocco G. 
Published: January 2005

AbstractThe presence of acetylcholinesterase has been reported in chick dorsal root ganglia at early developmental stages although acetylcholine is not known to play a role in these ganglia. Recently, we reported that during development the level of acetylcholinesterase increases continuously and the enzyme becomes gradually expressed in all sensory neurons. These observations prompted the study of the developmental pattern of expression of other cholinergic markers, such as choline acetyltransferase (ChAT) and the high affinity transport mechanism for choline. ChAT activity is barely detectable at early developmental stages (E7) and increases markedly thereafter, with an activity profile similar to that described for acetylcholinesterase. A similar increase in enzyme activity is also observed when ChAT is measured in dorsal root ganglia explants and in dissociated cells in culture. The study of ChAT activity in cultured cells shows an increase over a period of 3 days, thus ruling out the hypothesis that motor fibers, still associated to the ganglia, may represent a possible source of the enzyme. Immunostaining of whole ganglia or cultured cells shows that ChAT immunoreactivity is not restricted to a specific neuronal subpopulation but appears as a common marker of sensory neurons. High affinity choline uptake, blocked by hemicholinium, is present in sensory neurons cultured from E7 dorsal root ganglia. Observations on cultured neurons from later stages (E18) indicate that choline transport is not a transient property of sensory neurons. These observations show a similar pattern of expression of several cholinergic markers during development. Such a pattern is maintained at significant levels also in mature ganglia. © 1994 Wiley‐Liss, Inc.
Induction of glioma cell death by 1,25 (OH)2 vitamin D3: Towards an endocrine therapy of brain tumors?
Authors: Naveilhan P. , Berger F. , Haddad K. , Barbot N. , Benabid A.‐L. , Brachet P. , Wion D. 
Published: January 2005

AbstractThe secosteroid 1,25‐dihydroxyvitamin D3 (1,25 (OH)D2DD3 is the major biologically active metabolite of vitamin D. Antitumor activity of this hormone has been observed on several cell lines and on breast cancer in vivo. The purpose of this in vitro study was to determine the possible effect of 1,25(OH)2D3 on glioma cells. Two glioma cell lines from rat (C6) or human (GHD) origin were cultured in the presence of 1,25(OH)2D3. The sensitivity of these cells to 1,259OH)2D3 was assessed with a colorimetric MTT assay. A cytotoxic effect of 1,25(OH)2D3 was detected at concentrations around 10−8 M. A lag period of 3 days was required between the onset of the treatment and the observation of the effects. However, the continuous presence of 1,25(OH)2D3 is not required since cell death occurred even when C6 cells were challenged for 24 hr with 1,25(OH)2D3and then cultured in the absence of the hormone. In addition, 1,25(OH)D2D3 regulates the expression of its own recepors in C6 glioma. These results provide to our knowledge the first evidence for a cytotoxic effect of 1,25(OH)2D3 on rat and human glioma cells and could offer both an experimental model to study a programmed cell death in a brain‐derived cell line and a new strategy for the inhibition of glioma growth in vivo. © 1994 Wiley‐Liss, Inc.
Increased CNTF gene expression in process‐bearing astrocytes following injury is augmented by R(−)‐deprenyl
Authors: Seniuk N. A. , Henderson J. T. , Tatton W. G. , Roder J. C. 
Published: January 2005

AbstractR(−)‐deprenyl has been shown to rescue axotomixed immature facial motoneurons with an efficacy comparable to that of the neurotrophic factors CNTF and BDNF (Salo and Tatton, J Neurosci Res 31:394–400, 1992; Ansari et al., J Neurosci 13:4042–4053, 1393). Recent work has suggested that some of the actions of (−)‐deprenyl may be mediated through reactive astrocytes (Biagini et al., NeuroReport 4:955–958, 1993). To test this proposal we have developed an in vitro model of reactive gloisis consisting of a mixed astrocyte population of flat and process‐bearing (PB) astroglia taken from postnatal day (PD) 2 or PD5 rat cerebral cortex. After mechanical wounding, PB astrocytes preferentially migrate into the wound zone while flat astrocytes maintain their position at the wound edge. CNTF mRNA was localized to PB astrocytes, but not flat astrocytes, as determined by in situ hybridization using biotin‐labelled riboprobes. Following “wounding,” there was an increase in CNTF mRNA in PB astrocytes only, which could be further enhanced by a single pulse of (−)‐deprenyl (10−8−10−11 M) 48 hr after injury. (−)‐Deprenyl also increased the total process length of PB astrocytes after wounding by an average of 50%. The stereoisomer (+)‐deprenyl (10−9 M) had no effect on either astrocyte process length or CNTF mRNA content. This is the first report to our knowledge of an agent which can upregulate CNTF gene expression in astroglial cell culture as well as influence glial cell process length. We propose that some of the trophic‐like action of (−)‐deprenyl may be mediated through a specific subpopulation of astroglia. © Wiley‐Liss, Inc.
Cellular distribution of calbindin D28K mRNAs in the adult mouse brain
Authors: Frantz G. D. , Tobin A. J. 
Published: January 2005

AbstractWe have determined the cellular distribution of calbindin D28K mRNAs throughout the mouse brain by in situ hybridization. While these studies identified neuronal populations similar to those previously identified in rat brain by immunohistochemistry, some discrepanicies exist. These may derive from species differences or from the immunological cross‐reactivity of calbindin D28K antiserum with other proteins. We note an intriguing association between the distribution of neurons containing calbindin D28K mRNA and those reported by others to contain the inositol 1,4,5‐triphosphate (InsP3) receptor. © 1994 Wiley‐Liss, Inc.
Protein synthesis and mRNA in isolated growth cones from differentiating SH‐SY5Y neuroblastoma cells
Authors: Meyerson G. , Parrow V. , Gestblom C. , Johansson I. , Påhlman S. 
Published: January 2005

AbstractThe human neuroblastoma cell line, SH‐SY5Y, differentiates into a neuronal, sympathetic phenotype in the presence of phorbol ester and serum. Growth cones prepared from differentiating SH‐SY5Y cells have characteristics similar to those of growth cones from embryonic rat brain. In addition, SH‐SY5Y growth cones contain ribosomes. In this study we show, by metabolic labeling of isolated growth cones, that local protein syntheisis occurred in these structures. The pattern of labeled proteins was very similar to that of the corresponding cell body fraction. RNA was shown to be transported to the growth cone compartment, and by in situ hybridization. β‐actin mRNA could be visualized in intact neuritic growth cones. Comparison by Northern blot hybridizations of RNA prepared from growth cones and cell bodies, respectively, showed that mRNAs coding for growth‐associated protein 43, microtubule‐associated protein 2, actin, neuropeptide tyrosine, and glyceraldehyde‐3‐phosphate dehydrogenase were present in both fractions. In contrast, mRNAs coding for the nuclear proteins c‐jun and N‐myc were virtually absent in the growth cone, but readily detectable in the cell body preparation. The selective distribution of mRNAs to the growth cones was not restricted to stable, abundant mRNA species, since mRNA coding for the insulin‐like growth factor I receptor was stable, but not present in growth cones. Thus, differentiating SH‐SY5Y cells can sort and transport RNA to the growth cone compartment, suggesting that this system of clonal cells could be useful to unravel mechanisms involved in the compartmentalization of mRNA. © 1994 Wiley‐Liss, Inc.
Tenascin mRNA isoforms in the developing mouse brain
Authors: Dörries U. , Schachner M. 
Published: January 2005

AbstractThe extracellular matrix glycoprotein tenascin is expressed in the developing mouse cerebellum as a group of four protein species of different molecular weights. The difference is most likely due to alternative splicing which is known to occurr in tenascin mRNA isoforms that would account for this heterogeneity, tenascin splice variants were isolated from mouse brain by the polymerase chain reaction (PCR). In agreement with Northern blot analysis, amplification by PCR revealed a general decrease in tenascin mRNA expression during development from embryonic and early postnatal to adult stages. This decrease was more pronounced for isoforms of high molecular weight compared to those of low molecular weight. In accord with the observations at the protein level, four splice variants were found to be predominantly expressed, containing insertions of either six, five, or one fibronection type III repeat, or comprising no insertion. In addition, a minor splice variant with an insertion of four fibronectin type III repeats was isolated. Three of the isolated mRNA splice variants have not yet been described for mouse tenascin. Among them, an isoform containing six alternatively spliced repeats was found to include a novel fibronectin type III repeat. The sequence of this repeat displays 96.7% similarity to a corresponding type III repeat in human tenascin, revealing a strict evolutionary conservation between tenascin molecules from different species in the region of alternative splicing. Southern blot analysis of the amplified mRNA isoforms showed that the novel mouse type III repeat is confined to splice variants with an insertion of six fibronectin type III repeats. Furthermore, in situ hybridization on sections from mouse embryos indicated that tenascin‐specific mRNAs containing the novel type III repeat are predominantly expressed in the central nervous system. © 1994 Wiley‐Liss, Inc.
In vitro differentiation of E‐N‐CAM expressing rat neural precursor cells isolated by FACS during prenatal development
Authors: Blass‐Kampmann S. , Reinhardt‐Maelicke S. , Kindler‐Röhrborn A. , Cleeves V. , Rajewsky M. F. 
Published: January 2005

AbstractMost fetal rat brain cells expressing the embryonal, highly sialyated form of the cell adhesion molecule N‐CAM (E‐N‐CAM) are precursor cells, as jugded from the absence of marker molecules specific for mature neural cell types. However, the detection of E‐N‐CAM+ cells in frozen sections does not provide information on the lineage‐specific differentiation of these cells during development. To investigate their differentiation behaviour in vitro, E‐N‐CAM+ cells were isolated at different times of brain development by fluorescence‐activated cell sorting (FACS), using a monoclonal antibody (Mab RB21‐7) which specifically recognizes polysialic acid (PSA) residues on E‐N‐CAM. Double‐immunofluorescence analyses showed that ht emajority of E‐N‐CAM+ cells isolated on prenatal days 15 to 18 differentiated into neurons while a small subset of Mab RB21‐7 binding cells proved to be astrocytic precursors and/or bipotential. The proportion of E‐N‐CAM+ astrocytic precursors increased during later development (prenatal day 22) concomitantly with the onset of gliogenesis. While conversion of E‐N‐CAM to mature forms of N‐CAM was never observed in neurons during cultivation, E‐N‐CAM+ cells of the astrocyte lineage switched to N‐CAM soon after the onset of GFAP expression. A lineage‐specific transition of E‐N‐CAM to mature N‐CAM expression is, therefore, suggested for these astrocytic progenitor cells during rat brain development. © 1994 Wiley‐Liss, Inc.