Abstract
We demonstrate that hCD4-primed gp120IIIB interacts with CXCR4 receptors expressed by postnatal mouse neural progenitor cells and elicits robust Ca 2+ signals. The chemokine SDF-1 acted as a chemoattractant and a mitogenic stimulus for these neural progenitor cells. Although hCD4/gp120 was not able to produce chemoattraction or increase proliferaton, it completely blocked the ability of SDF-1 to produce these effects. Thus, gp120 can act both as an agonist and de facto antagonist of CXCR4-mediated signaling in neural progenitor cells. It is possible that the ability of hCD4/gp120 to block SDF-1 signaling in neural progenitors may contribute to the neuropathological effects of HIV-1.
Original language | English (US) |
---|---|
Pages (from-to) | 68-76 |
Number of pages | 9 |
Journal | Journal of Neuroimmunology |
Volume | 160 |
Issue number | 1-2 |
DOIs | |
State | Published - Mar 2005 |
Funding
Supported by NIH grants NS043095, DA013141 and MH040165.
Keywords
- Chemokines
- Dementia
- HIV-1
- Migration
- Neural stem cells
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology