GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com

TableEdit

Jump to: navigation, search

PMID:12753088

You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor

Citation

Eugenin, EA, D'Aversa, TG, Lopez, L, Calderon, TM and Berman, JW (2003) MCP-1 (CCL2) protects human neurons and astrocytes from NMDA or HIV-tat-induced apoptosis. J. Neurochem. 85:1299-311

Abstract

Acquired immunodeficiency syndrome (AIDS)-associated dementia is often characterized by chronic inflammation, with infected macrophage infiltration of the CNS resulting in the production of human immunodeficiency virus type 1 (HIV-1) products, including tat, and neurotoxins that contribute to neuronal loss. In addition to their established role in leukocyte recruitment and activation, we identified an additional role for chemokines in the CNS. Monocyte chemoattractant protein-1 (MCP-1 or CCL2) and regulated upon activation normal T cell expressed and secreted (RANTES) were found to protect mixed cultures of human neurons and astrocytes from tat or NMDA-induced apoptosis. Neuronal and astrocytic apoptosis in these cultures was significantly inhibited by co-treatment with MCP-1 or RANTES but not IP-10. The protective effect of RANTES was blocked by antibodies to MCP-1, indicating that RANTES protection is mediated by the induction of MCP-1. The NMDA blocker, MK801, also abolished the toxic effects of both tat and NMDA. Tat or NMDA treatment of mixed cultures for 24 h resulted in increased extracellular glutamate ([Glu]e) and NMDA receptor 1 (NMDAR1) expression, potential contributors to apoptosis. Co-treatment with MCP-1 inhibited tat and NMDA-induced increases in [Glu]e and NMDAR1, and also reduced the levels and number of neurons containing intracellular tat. These data indicate that MCP-1 may play a novel role as a protective agent against the toxic effects of glutamate and tat.

Links

PubMed

Keywords

AIDS Dementia Complex/metabolism; Apoptosis/drug effects; Astrocytes/cytology; Astrocytes/drug effects; Astrocytes/physiology; Cells, Cultured; Chemokine CCL2/pharmacology; Chemokine CCL5/pharmacology; Coculture Techniques; Dizocilpine Maleate/pharmacology; Excitatory Amino Acid Antagonists/pharmacology; Gene Products, tat/toxicity; Glutamic Acid/metabolism; Humans; N-Methylaspartate/toxicity; Neurons/cytology; Neurons/drug effects; Neurons/physiology; Neuroprotective Agents/pharmacology; Receptors, N-Methyl-D-Aspartate/metabolism; tat Gene Products, Human Immunodeficiency Virus

public



Cancel