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

M. T. Corasaniti, S. Piccirilli, A. Paoletti, R. Nisticò, A. Stringaro, W. Malorni, A. Finazzi-Agrò, G. Bagetta

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)67-70
Number of pages4
JournalNeuroscience Letters
Volume312
Issue number2
DOIs
Publication statusPublished - Oct 19 2001

Keywords

  • Apoptosis
  • Chemokine receptors
  • Chemokines
  • HIV-1 gp120
  • IL-1β

ASJC Scopus subject areas

  • Neuroscience(all)

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