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Tumor necrosis factor-α: A potentially neurodestructive cytokine produced by glia in the human glaucomatous optic nerve head
Glia, 2000-10, Vol.32 (1), p.42-50
Yuan, Liya
Neufeld, Arthur H.
2000
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Yuan, Liya
Neufeld, Arthur H.
Titel
Tumor necrosis factor-α: A potentially neurodestructive cytokine produced by glia in the human glaucomatous optic nerve head
Ist Teil von
Glia, 2000-10, Vol.32 (1), p.42-50
Ort / Verlag
New York: John Wiley & Sons, Inc
Erscheinungsjahr
2000
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Tumor necrosis factor‐α (TNF‐α) mediates a range of cellular responses, which have potentially detrimental consequences that affect multiple cell types. To determine whether TNF‐α contributes to glaucomatous optic neuropathy, we have studied the expression of this cytokine and its receptor, tumor necrosis factor receptor‐1 (TNF‐ R1), in human glaucomatous optic nerve heads from patients with different stages of disease using double labeling fluorescence immunohistochemistry. We have also investigated the ability of this cytokine to induce nitric oxide synthase (NOS‐2) in cultured human optic nerve astrocytes by immunocytochemistry and immunoblot. Normal tissue showed constitutive expression of TNF‐R1 in the vasculature of the optic nerve heads but no positive labeling for TNF‐α. In the glaucomatous optic nerve heads, the expression of both TNF‐α and TNF‐R1 were apparently upregulated, primarily in glial fibrillary acidic protein (GFAP)‐positive astrocytes, and appeared to parallel the progression of optic nerve degeneration. In eyes with severe glaucomatous damage, some HLA‐DR positive microglia also contained TNF‐α and TNF‐R1. In the most severely damaged optic nerve heads, the axons of the retinal ganglion cells contained TNF‐R1 and, therefore, are direct targets for neurodegeneration caused by TNF‐α. In vitro astrocytes constitutively express TNF‐R1 and TNF‐α stimulation induces expression of NOS‐2. We hypothesize that TNF‐α contributes to the progression of optic nerve degeneration in glaucoma by both a direct effect on the axons of the retinal ganglion cells and by inducing NOS‐2 in astrocytes. GLIA 32:42–50, 2000. © 2000 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0894-1491
eISSN: 1098-1136
DOI: 10.1002/1098-1136(200010)32:1<42::AID-GLIA40>3.0.CO;2-3
Titel-ID: cdi_proquest_miscellaneous_18019317
Format
–
Schlagworte
Aged
,
Aged, 80 and over
,
astrocyte
,
Astrocytes - metabolism
,
Astrocytes - pathology
,
Biological and medical sciences
,
Cells, Cultured
,
glaucoma
,
Glaucoma - metabolism
,
Glaucoma - pathology
,
Glaucoma - physiopathology
,
Glaucoma and intraocular pressure
,
Humans
,
inducible nitric oxide synthase
,
Medical sciences
,
microglia
,
Middle Aged
,
Neuroglia - metabolism
,
Neuroglia - pathology
,
Neurotoxins - adverse effects
,
Neurotoxins - metabolism
,
Nitric Oxide - adverse effects
,
Nitric Oxide - metabolism
,
Nitric Oxide Synthase - adverse effects
,
Nitric Oxide Synthase - metabolism
,
Nitric Oxide Synthase Type II
,
Ophthalmology
,
Optic Disk - metabolism
,
Optic Disk - pathology
,
Optic Disk - physiopathology
,
Optic Nerve Diseases - etiology
,
Optic Nerve Diseases - pathology
,
Optic Nerve Diseases - physiopathology
,
Receptors, Tumor Necrosis Factor - metabolism
,
Retinal Ganglion Cells - metabolism
,
Retinal Ganglion Cells - pathology
,
TNF receptor
,
Tumor Necrosis Factor-alpha - adverse effects
,
Tumor Necrosis Factor-alpha - metabolism
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