Role of activated astrocytes in neuronal damage: Potential links to HIV-1-associated dementia

Autor: Raisa Persidsky, Anuja Ghorpade, Jialin C. Zheng, Li Wu, Kathleen Borgmann, Muralidhar S. Deshpande, Courtney N. Schellpeper
Rok vydání: 2005
Předmět:
Fas Ligand Protein
Indoles
Central nervous system
Glutamic Acid
Tetrazolium Salts
Apoptosis
Cell Count
Enzyme-Linked Immunosorbent Assay
Nerve Tissue Proteins
Toxicology
Nestin
Fetus
Intermediate Filament Proteins
Neurofilament Proteins
Glial Fibrillary Acidic Protein
In Situ Nick-End Labeling
medicine
Humans
Drug Interactions
Cells
Cultured
Caspase
Neurons
Analysis of Variance
Membrane Glycoproteins
biology
Glial fibrillary acidic protein
Tumor Necrosis Factor-alpha
General Neuroscience
Neurodegeneration
Neurotoxicity
medicine.disease
Immunohistochemistry
Astrogliosis
Thiazoles
medicine.anatomical_structure
Gene Expression Regulation
Astrocytes
Caspases
Culture Media
Conditioned
biology.protein
Tumor necrosis factor alpha
Microtubule-Associated Proteins
Neuroscience
Interleukin-1
Astrocyte
Zdroj: Neurotoxicity Research. 7:183-192
ISSN: 1476-3524
1029-8428
DOI: 10.1007/bf03036448
Popis: HIV-1-associated dementia (HAD) is an important complication of HIV-1 infection. Reactive astrogliosis is a key pathological feature in HAD brains and in other central nervous system (CNS) diseases. Activated astroglia may play a critical role in CNS inflammatory diseases such as HAD. In order to test the hypothesis that activated astrocytes cause neuronal injury, we stimulated primary human fetal astrocytes with HAD-relevant pro-inflammatory cytokine IL-1beta. IL-1beta-activated astrocytes induced apoptosis and significant changes in metabolic activity in primary human neurons. An FITC-conjugated pan-caspase inhibitor peptide FITC-VAD-FMK was used for confirming caspase activation in neurons. IL-1beta activation enhanced the expression of death protein FasL in astrocytes, suggesting that FasL is one of the potential factors responsible for neurotoxicity observed in HAD and other CNS diseases involving glial inflammation. Our data presented here add to the developing picture of role of activated glia in HAD pathogenesis.
Databáze: OpenAIRE
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