Chemokines Released from Astroglia by Vasoactive Intestinal Peptide: Mechanism of Neuroprotection from HIV Envelope Protein Toxicity
| Autor: | Janet Hauser, Douglas E. Brenneman, Catherine Y. Spong, Terry M. Phillips |
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| Rok vydání: | 2006 |
| Předmět: |
Chemokine
Programmed cell death Cell Survival Vasoactive intestinal peptide Inflammation Stimulation HIV Envelope Protein gp120 Neuroprotection Antibodies General Biochemistry Genetics and Molecular Biology History and Philosophy of Science Neutralization Tests medicine Animals Chemokine CCL4 Receptor Chemokine CCL5 Cells Cultured Cell Death biology Chemistry General Neuroscience Neurotoxicity Macrophage Inflammatory Proteins medicine.disease Rats Cell biology Neuroprotective Agents Astrocytes Chemokines CC Immunology biology.protein Chemokines medicine.symptom Vasoactive Intestinal Peptide |
| Zdroj: | Annals of the New York Academy of Sciences. 921:109-114 |
| ISSN: | 1749-6632 0077-8923 |
| DOI: | 10.1111/j.1749-6632.2000.tb06956.x |
| Popis: | The mechanism through which VIP prevents neurotoxicity associated with HIV envelope protein has been shown to involve the release of a beta-chemokine, MIP-1 alpha. Astrocytes stimulated with subnanomolar concentrations of VIP caused the release of MIP-1 alpha 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-1 alpha like substance is necessary for neuronal survival and interference with this action results in neuronal cell death. |
| Databáze: | OpenAIRE |
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