Evidence that the HIV-1 coat protein gp120 causes neuronal apoptosis in the neocortex of rat via a mechanism involving CXCR4 chemokine receptor

The HIV-1 coat protein, gp120 (100 ng given intracerebroventricularly (i.c.v.) daily for seven consecutive days) causes DNA fragmentation in the brain neocortex of rat. In neocortical cells bearing ultrastructural features typical of apoptosis, electron microscopy revealed specific immunopositivity...

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Bibliographic Details
Published in:Neuroscience letters 2001-10, Vol.312 (2), p.67-70
Main Authors: Corasaniti, M.T, Piccirilli, S, Paoletti, A, Nisticò, R, Stringaro, A, Malorni, W, Finazzi-Agrò, A, Bagetta, G
Format: Article
Language:English
Subjects:
Ageing, cell death
AIDS Dementia Complex - metabolism
AIDS Dementia Complex - pathology
AIDS Dementia Complex - physiopathology
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - immunology
Biological and medical sciences
Cell physiology
Chemokine CXCL12
Chemokine receptors
Chemokines
Chemokines, CXC - immunology
Chemokines, CXC - pharmacology
Dose-Response Relationship, Drug
Fundamental and applied biological sciences. Psychology
Glial Fibrillary Acidic Protein - metabolism
HIV Envelope Protein gp120 - immunology
HIV Envelope Protein gp120 - pharmacology
HIV-1 - immunology
HIV-1 - pathogenicity
HIV-1 gp120
IL-1β
Immunohistochemistry
In Situ Nick-End Labeling
Interleukin-1 - immunology
Interleukin-1 - metabolism
Male
Microglia - cytology
Microglia - immunology
Microglia - metabolism
Microscopy, Electron
Molecular and cellular biology
Neocortex - drug effects
Neocortex - pathology
Neocortex - ultrastructure
Nerve Degeneration - chemically induced
Nerve Degeneration - pathology
Nerve Degeneration - physiopathology
Neurofilament Proteins - metabolism
Neurons - drug effects
Neurons - pathology
Neurons - ultrastructure
Neurotoxins - immunology
Neurotoxins - pharmacology
Rats
Rats, Wistar
Receptors, CXCR4 - drug effects
Receptors, CXCR4 - immunology
Receptors, CXCR4 - metabolism
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Summary:The HIV-1 coat protein, gp120 (100 ng given intracerebroventricularly (i.c.v.) daily for seven consecutive days) causes DNA fragmentation in the brain neocortex of rat. In neocortical cells bearing ultrastructural features typical of apoptosis, electron microscopy revealed specific immunopositivity for neurofilament cytoskeletal proteins, suggesting the neuronal nature of dying cells. Neuronal apoptosis by gp120 implicates CXCR4 chemokine receptors; in fact, in rats receiving a single daily, non-neurotoxic, dose of SDF-1α (0.25 pmoles given i.c.v. for 7 days before gp120), the natural ligand of CXCR4 receptor, apoptosis was significantly hindered. The mechanism of SDF-1α protection involves inhibition of gp120-enhanced expression of IL-1β, a cytokine implicated in the mechanisms of apoptosis induced by the viral protein in the neocortex of rat.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(01)02191-7