Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Neurosci. 2009;119(2):157-65. doi: 10.1080/00207450802335537.

Mitochondria influence Fas expression in gp120-induced apoptosis of neuronal cells.

Author information

1
Immunobiology Center, Mount Sinai School of Medicine, New York, NY, USA. sunthoma@utmb.edu

Abstract

The human immunodeficiency virus-1 (HIV-1) destroys the immune system and also induces neurological disease culminating into dementia (HIV-associated dementia). Though the HIV viral protein gp120 induces apoptosis in neuronal cells, the mechanism of action is still poorly defined. Recent studies show that cells die during apoptosis by Fas aggregation aided by the mitochondrial proapoptotic proteins. Our studies show an increase in expression of Fas and its associated downstream proteins after treatment of the neuroblastoma cells, SH-SY5Y, with gp120. Fas and its associated death proteins, FADD and caspase-8 (DISC), are downregulated when treated with the caspase inhibitors. The results indicate that mitochondrial-death proteins like caspases may influence the upregulation of the death receptor Fas, and the inhibition of caspases prevents gp120-induced apoptosis.

PMID:
19125371
DOI:
10.1080/00207450802335537
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center