Mechanisms of prionSc- and HIV-1 gp120 induced neuronal cell death.
In vitro experiments revealed that the scrapie prion protein, PrP(Sc), as well as the PrP fragment PrP106-126, and the HIV-1 coat protein gp120 induce apoptosis of rat cortical neurons. The toxic effect displayed by PrP and gp120 could be blocked by NMDA receptor antagonists. Treatment of neuronal cells with PrP106-126 resulted in a drop of intracellular glutathione level and changes in the level of Bcl-2. Evidence is presented that gp120 causes an activation of phospholipase A2, resulting in the increased release of arachidonic acid, which may in turn sensitize the NMDA receptor.
Schröder
H C
HC
Institut für Physiologische Chemie, Abteilung Angewandte Molekularbiologie, Universität, Mainz, Germany.
Perovic
S
S
Kavsan
V
V
Ushijima
H
H
Müller
W E
WE
D000818:Animals; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D015699:HIV Envelope Protein gp120 / Q000633:toxicity*; D006801:Humans; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018620:PrPSc Proteins / Q000633:toxicity*; D051381:Rats
D015699:HIV Envelope Protein gp120; D018620:PrPSc Proteins