The mechanism through which VIP prevents neurotoxicity associated with HIV envelope protein has been shown to involve the release of a βchemokine, MIP-1α. Astrocytes stimulated with subnanomolar concentrations of VIP caused the release of MIP-1α and RANTES, both of which have been shown to prevent neuronal cell death associated with gp120. It is further proposed that gp120 causes neuronal cell death, in part, by competing with endogenous chemokines at various chemokines receptors in the brain that are necessary for neuronal survival. Although the chemokines are known to be mediators of inflammation, our studies suggest that these compounds have additional roles as neuroprotective agents that depend on the concentration of chemokine, cellular microenvironment, and stage of development of target neurons. Our studies further imply that in a developing system, stimulation with a MIP-1α like substance is necessary for neuronal survival and interference with this action results in neuronal cell death.
|Original language||English (US)|
|Number of pages||6|
|Journal||Annals of the New York Academy of Sciences|
|State||Published - Dec 2000|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science