Can proline-rich polypeptide complex mimic the effect of nerve growth factor?
PBN-AR
Instytucja
Instytut Immunologii i Terapii Doświadczalnej im. Ludwika Hirszfelda Polskiej Akademii Nauk
Informacje podstawowe
Główny język publikacji
EN
Czasopismo
Biofactors
ISSN
0951-6433
EISSN
1872-8081
Wydawca
Amsterdam : Ios Press
Rok publikacji
2014
Numer zeszytu
5
Strony od-do
501-512
Numer tomu
40
Identyfikator DOI
Liczba arkuszy
Słowa kluczowe
EN
proline-rich polypeptide complex (PRP)
nonapeptide (NP)
nerve growth factor
nitric oxide
cyclic GMP
ERK1/2 kinases
Streszczenia
Język
EN
Treść
Naturally occurring compounds that can act as prosurvival factors and neurite formation stimulants in the conditions of reduced neurotrophins production are important both in neuronal protection and therapy of neurodegenerative disorders. Therefore, the role of proline-rich polypeptide complex (PRP) and its nonapeptide fragment (NP) in the promotion of pheochromocytoma cell line (PC12) survival and neurite outgrowth pathway is presented. It was shown that PRP/NP did not affect the neuronal nitric oxide synthase (nNOS) at the transcriptional and protein level. However, the activity of nNOS and intracellular nitric oxide (NO) concentration was markedly increased after treatment of PC12 cells with peptides. This reaction was inhibited by l-NAME—nNOS inhibitor. It was shown that PRP and NP induce the soluble guanylyl cyclase to release higher amount of cyclic GMP (cGMP), and subsequently, the increased phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) is observed. This effect was abolished by both U0126 (inhibitor of ERK1/2) and also by l-NAME. Reduction of ERK1/2 activity observed in the presence of nNOS inhibitor suggests that its activation is NO-dependent. The presented results shed some light on the mechanism of action of PRP complex. PRP and NP can activate NO/cGMP/ERK1/2 signaling pathway, similarly to nerve growth factor (NGF). The prosurvival action and short fibers formation suggest the role of PRP and NP in neuroprotection and the initiation of neuritogenesis. They can also participate in the amplification of signals controlling the survival and differentiation of neurons effect when the deficit of NGF takes place. © 2014 BioFactors, 40(5):501–512, 2014
Cechy publikacji
artykuł oryginalny
Inne
System-identifier
PX-56b48bcb8106eb71826f81bd
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