AIDSWEEKLY Plus; Monday, June 2, 2003
Staff Medical Writers
According to recent research from Italy, "the human CHP100 neuroblastoma cell line has been shown to provide an useful in vitro model to elucidate the mechanisms underlying HIV-1 gp120 neurotoxicity."
Using this model, M.T. Corasaniti and coauthors at the University of Magna Graecia found "evidence demonstrating that exposure to a cytotoxic concentration of the viral coat protein upregulates expression of the inducible isoform of cyclooxygenase (COX-2) in neuroblastoma cells".
This effect "seems to be due to the previously observed increase in secreted IL-1beta," they noted. Moreover, study results revealed that "acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of interleukin-1 converting enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death."
"In addition, NS-398, a selective inhibitor of COX-2 activity, affords neuroprotection strengthening the role of COX-2 in the mechanisms of death," according to the report.
These findings "support the notion that IL-1beta is the signal through which gp120 elevates COX-2 expression," and that "the latter is strongly implicated in the mechanisms underlying cytotoxicity," the researchers concluded.
Corasaniti and colleagues published their study in Toxicology Letters (Caspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells. Toxicol Lett 2003 Apr 4;139(2-3):213-9.
For additional information, contact M.T. Corasaniti, University of Magna Graecia, Faculty of Pharmacy, Department of Pharmacobiological Science, Complesso Nini Barbieri, I-88021 Catanzaro, Italy.
Publisher contact information for the journal Toxicology Letters is: Elsevier Science Ireland Ltd., Customer Relations Manager, Bay 15, Shannon Industrial Estate, Co. Clare, Ireland.
The information in this article comes under the major subject areas of AIDS and HIV, Enzymology, Neurotoxin and Proteomics.
This article was prepared by AIDS Weekly editors from staff and other reports.
Reference
Corasaniti MT, Bellizzi C, Russo R, et al., "Caspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells", Toxicol Lett 2003 Apr 4;139(2-3):213-9.
PubMED Related articles Search
030602
AW030602
Copyright © 2003 - Charles Henderson, Publisher. All rights Reserved. Permission to reproduce granted to AEGIS by Charles W. Henderson. Authorization to reproduce for personal use granted granted by C. W. Henderson, Publisher, provided that the fee of US$4.50 per copy, per page is paid directly to the Copyright Clearance Center, 27 Congress Street, Salem, Massachusetts 01970, USA. Published by Charles Henderson, Publisher. Editorial & Publishing Office: P.O. Box 5528, Atlanta, GA 30307-0528 / Telephone: (800) 633-4931; Subscription Office: P.O. Box 830409, Birmingham, AL 35283-0409 / FAX: (205) 995-1588 http://www.newsrx.net
AEGiS is made possible through unrestricted grants from Boehringer Ingelheim, iMetrikus, Inc., the National Library of Medicine, and donations from users like you. Always watch for outdated information. This article first appeared in 2003. This material is designed to support, not replace, the relationship that exists between you and your doctor.
AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.
Copyright © 1980,2003. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content.