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  • 1
    Electronic Resource
    Electronic Resource
    A Cellular Stress Model for the Sequestration of Redox-Active Glial Iron in the Aging and Degenerating Nervous System (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 64 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The mechanisms responsible for the accumulation of redox-active brain iron in normal senescence and in Parkinson's disease remain poorly understood. The aminothiol compound cysteamine (CSH) induces the appearance of autofluorescent, iron-rich cytoplasmic granules in cultured astroglia that are identical to glial inclusions that progressively accumulate in the aging periventricular brain. Both in situ and in culture, these glial inclusions appear to arise in the context of a generalized cellular stress (heat shock) response. Several laboratories have previously concluded that porphyrins and heme ferrous iron are responsible, respectively, for red-orange autofluorescence and nonenzymatic peroxidase activity in the glial inclusions. In the present study we found that, contrary to hypothesis, CSH suppresses the incorporation of the heme precursors δ-amino[14C]levulinic acid and [14C]glycine into astroglial porphyrin and heme in primary culture. Similar results were obtained when the cells were preloaded with radiolabeled heme precursors for 24 h before CSH treatment, suggesting that the latter directly inhibits porphyrin-heme biosynthesis rather than limiting precursor uptake by these cells. We also demonstrated that CSH exposure results in the sequestration of iron-59 by astroglial mitochondria (granule precursors). The results of this study suggest that stress-related trapping of nonheme iron by astroglial mitochondria may be an important mechanism underlying the pathological accumulation of redox-active iron in the basal ganglia of subjects with Parkinson's disease. CSH-treated astrocytes provide a useful model to investigate the role of stress-related dysregulation of neuroglial iron metabolism in the aging and degenerating nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.64041868.x
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  • 2
    Electronic Resource
    Electronic Resource
    Role of the Cellular Stress Response in the Biogenesis of Cysteamine-Induced Astrocytic Inclusions in Primary Culture (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Cysteamine (CSH; 2-mercaptoethylamine) stimulates the accumulation of peroxidase-positive inclusions in cultured astroglia akin to those observed in the aging periventricular brain. Because CSH induces the synthesis of a stress protein (heme oxygenase) in rat liver, we hypothesized that aspects of the cellular stress response may play a role in the biogenesis of CSH-induced astro-cyte granules. In the present study, we performed indirect immunofluorescent staining and immunoblotting for various stress proteins in rat neuroglial cultures. Exposure of astrocyte cultures to CSH enhanced immunostaining for heme oxygenase-1 (HO-1) and heat-shock proteins 27, 72, and 90, but not glucose-regulated protein 94, relative to untreated cultures. CSH-pretreated astrocytes exhibited enhanced tolerance to H2O2 toxicity relative to untreated cells, providing physiological evidence of an antecedent stress response in the former. In addition, exposure for 12 days to H2O2, a known inducer of the stress response, elicited astrocyte granulation similar to that observed with CSH. Chronic induction of HO-1 and other stress proteins may participate in the biogenesis of metal-loporphyrin-rich inclusions in CSH-treated astroglial cultures and in astrocytes of the aging periventricular brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb09813.x
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  • 3
    Electronic Resource
    Electronic Resource
    Astroglial cytoprotection by erythropoietin pre-conditioning: implications for ischemic and degenerative CNS disorders (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 93 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Erythropoietin (Epo) is a glycoprotein secreted by the kidney in response to hypoxia that stimulates erythropoiesis through interaction with cell surface Epo receptors. Pre-treatment with Epo has been shown to protect neurons in models of ischemic injury. The mechanism responsible for this neuroprotection and the effects of Epo on astroglial and other non-neuronal cell populations remain unknown. In the present study, we determined whether Epo pre-treatment protects neonatal rat astrocytes from apoptotic cell death resulting from treatment with nitric oxide, staurosporine (STS) and arsenic trioxide and possible mechanisms mediating Epo-related cytoprotection. Epo (5–20 U/mL) significantly attenuated multiple hallmarks of apoptotic cell death in astroglia exposed to nitric oxide and STS but not arsenic trioxide. Epo (20 U/mL) induced mild oxidative stress as shown by increases in heme oxygenase (HO)-1 mRNA and protein expression that could be suppressed by antioxidant coadministration. Moreover, coincubation with tin-mesoporphyrin, a competitive inhibitor of HO activity, abrogated the cytoprotective effects of Epo (20 U/mL) in the face of STS treatment. Thus, induction of the ho-1 gene may contribute to the glioprotection accruing from high-dose Epo exposure. Epo may augment astroglial resistance to certain chemical stressors by oxidative stress-dependent and -independent mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03038.x
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  • 4
    Electronic Resource
    Electronic Resource
    Increased T-type Ca2+ channel activity as a determinant of cellular toxicity in neuronal cell lines expressing polyglutamine-expanded human androgen receptors (2000)
    Springer
    Molecular and cellular biochemistry 203 (2000), S. 23-31 
    Details
    ISSN: 1573-4919
    Keywords: T-type Ca2+ channel ; polyglutamine-expanded androgen receptor ; CAG trinucleotide repeats ; spinobulbar muscular atrophy ; apoptosis ; motorneuron ; cell lines ; neuroblastoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have analyzed Ca2+ currents in two neuroblastoma-motor neuron hybrid cell lines that expressed normal or glutamine-expanded human androgen receptors (polyGln-expanded AR) either transiently or stably. The cell lines express a unique, low-threshold, transient type of Ca2+ current that is not affected by L-type Ca2+ channel blocker (PN 200-110), N-type Ca2+ channel blocker (ω-conotoxin GVIA) or P-type Ca2+ channel blocker (Agatoxin IVA) but is blocked by either Cd2+ or Ni2+. This pharmacological profile most closely resembles that of T-type Ca2+ channels [1-3]. Exposure to androgen had no effect on control cell lines or cells transfected with normal AR but significantly changed the steady-state activation in cells transfected with expanded AR. The observed negative shift in steady-state activation results in a large increase in the T-type Ca2+ channel window current. We suggest that Ca2+ overload due to abnormal voltage-dependence of transient Ca2+ channel activation may contribute to motor neuron toxicity in spinobulbar muscular atrophy (SBMA). This hypothesis is supported by the additional finding that, at concentrations that selectively block T-type Ca2+ channel currents, Ni2+ significantly reduced cell death in cell lines transfected with polyGln-expanded AR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007010020228
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  • 5
    Electronic Resource
    Electronic Resource
    Composition of Gomori-positive inclusions in astrocytes of the hypothalamic arcuate nucleus (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 240 (1994), S. 407-415 
    Details
    ISSN: 0003-276X
    Keywords: Astrocytes ; Gomori glia ; Autophagocytosis ; Metals ; Residual bodies ; Mitochondria ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Background: Astrocytes within the hypothalamic arcuate nucleus contain Gomori-positive inclusions that exhibit a nonenzymatic peroxidase activity. The source and composition of these Gomori-positive inclusions are currently unknown. Recent evidence, derived from cultured astrocytes, suggests that Gomori-positive inclusions may consist of autophagocytized accumulations of altered mitochondria and that the peroxidase activity is generated by iron or other metals which accumulate in these mitochondria.Methods: The present study applies electron microscopy, energy dispersive X-ray microanalysis, and immunocytochemistry in conjunction with confocal microscopy to determine the structure and composition of Gomori-positive inclusions in vivo.Results: The results indicate that Gomori-positive inclusions are heterogeneous structures often associated with microtubules and that they contain conspicuous mitochondrial components. Gomori-positive inclusions exhibit X-ray emission peaks for copper and, less often, chromium, either of which could account for the peroxidase activity.Conclusions: These results support the hypothesis that Gomori-positive inclusions are autophagosomes in which mitochondria are prominent. © 1994 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092400313
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