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C-terminal peptide of [gama]-enolase impairs amyloid-ß-induced apoptosis p75[sup](NTR) signaling
Pišlar, Anja (Author), Kos, Janko (Author)

URLURL - Presentation file, Visit http://link.springer.com/article/10.1007%2Fs12017-013-8247-9 This link opens in a new window

Abstract
[Gama]-enolase acts as a neurotrophic-like factor promoting growth, differentiation, survival and regeneration of neurons. It is shown in this study to exert a protective effect against amyloid-ß-peptide (Aß)-induced neurotoxicity in rat pheochromocytoma PC12 cells. Aß-induced toxicity was abolished in the presence of the active C-terminal peptide of Ž-enolase ([gama]-Eno) as measured by cell viability, lactate dehydrogenase release, sub G-1cell population, intracellular reactive oxygen species, mitochondrial functions and apoptotic morphology. [gama]-eno caused downregulation of the pro-apoptotic protein Bax and upregulation of the anti-apoptotic protein Bcl-2, as well as reduced caspase-3 activation. Exposure to Aß increased surface expression of p75 neurotrophin receptor (p75NTR), and the increase was abolished in the presence of [gama]-eno peptide. Further, pretreatment with [gama]-eno suppressed the activation of mitogen-activated protein kinases p38 and Jun-N-terminal kinase, which are p75NTR downstream effectors in apoptotic signaling. Moreover, AŽ triggered Ž-enolase co-immunoprecipitation with p75NTR as well as their strong association in the perimembrane region as shown by confocal microscopy, which further supports the interaction between these two proteins in cells insulted by Aß peptide. Our results indicate the possible use of [gama]-enolase C-terminal peptide for treating or preventing Alzheimer's disease.

Language:English
Keywords:gama enolaze, apoptoza, p75 nevrotrofin, Alzheimerjeva bolezen, nevrodegeneracija, zdravljenje
Work type:Not categorized (r6)
Tipology:1.01 - Original Scientific Article
Organization:FFA - Faculty of Pharmacy
Year:2013
Number of pages:str. 623-635
Numbering:Vol. 15, iss. 3
UDC:577.2:615.2
ISSN on article:1535-1084
DOI:10.1007/s12017-013-8247-9 Link is opened in a new window
COBISS.SI-ID:3492209 Link is opened in a new window
Views:527
Downloads:159
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Record is a part of a journal

Title:Neuromolecular medicine
Shortened title:Neuromol. med.
Publisher:Humana Press
ISSN:1535-1084
COBISS.SI-ID:21126951 This link opens in a new window

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