Effect of HIV-1 Gp41 Peptide on Expression and Metabolism of Amyloid Precursor Protein in Human Astroglioma Cell.
- Author:
Young Hae CHONG
1
;
Hae Kyung PARK
Author Information
1. Department of Microbiology, College of Medicine, Division of Molecular Biology, Ewha Medical Center, Ewha Womans University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
HIV-1 gp41 peptide;
AIDS dementia complex (ADC);
Soluble Amyloid Precursor Protein (sAPP);
Astroglial cells
- MeSH:
Amyloid*;
Astrocytoma*;
Brain;
Cell Line;
Central Nervous System;
Dementia;
Down-Regulation;
HIV Infections;
HIV-1*;
Humans*;
Metabolism*;
Neuroglia;
Neurons;
RNA, Messenger;
Transforming Growth Factor beta
- From:Journal of the Korean Society for Microbiology
1997;32(2):245-254
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Significant neurodegeneration leading to neurocognitive disorder and dementia has been observed in the central nervous system (CNS) of patients with HIV infection. Part of the neurodegenerative cascade in AIDS dementia may involve glial cells, perhaps through inhibiting the release of glial factors that protect neurons from variety of insults. Here, in an effort to find the mediators of HIV-induced brain damage, we examined the possible effect of a HIV-1 transmenbrane protein gp41 peptide (583-599) on expression and metabolism of amyloid precursor protein (APP) using human astroglial cell line. RT-PCR analysis demonstrated that gp 41 peptide did not significantly change expression patterns of APP mRNAs in lipopolysaccharide (LPS) activated astroglial cells for 6h. In contrast, gp41 peptide remarkably downregulated the level of secreted from of APP (sAPPa), which has been recently demonstrated as a potent neuroprotective factor. The reverse peptide, used as control had no such effect. The mechanism of gp41 peptide-induced down regulation of sAPPa production appears to be TGF-beta independent. These results implicate that gp41 peptide could be one of the mediator involved in the modulation of APP secretion within CNS, possibly contributing to the neuronal degeneration in HIV-1 associated neurological disease.
