| Autor: |
Neumann JR; AG Entwicklungsneurobiologie, Fakultät für Biologie und Biotechnologie, ND 6/72, Ruhr-Universität, 44801, Bochum, Germany., Dash-Wagh S, Jüngling K, Tsai T, Meschkat M, Räk A, Schönfelder S, Riedel C, Hamad MI, Wiese S, Pape HC, Gottmann K, Kreutz MR, Wahle P |
| Jazyk: |
angličtina |
| Zdroj: |
Brain structure & function [Brain Struct Funct] 2015 Jul; Vol. 220 (4), pp. 1935-50. Date of Electronic Publication: 2014 Apr 13. |
| DOI: |
10.1007/s00429-014-0764-2 |
| Abstrakt: |
The 30-amino acid peptide Y-P30, generated from the N-terminus of the human dermcidin precursor protein, has been found to promote neuronal survival, cell migration and neurite outgrowth by enhancing the interaction of pleiotrophin and syndecan-3. We now show that Y-P30 activates Src kinase and extracellular signal-regulated kinase (ERK). Y-P30 promotes axonal growth of mouse embryonic stem cell-derived neurons, embryonic mouse spinal cord motoneurons, perinatal rat retinal neurons, and rat cortical neurons. Y-P30-mediated axon growth was dependent on heparan sulfate chains. Y-P30 decreased the proportion of collapsing/degenerating growth cones of cortical axons in an Src and ERK-dependent manner. Y-P30 increased for 90 min in axonal growth cones the level of Tyr418-phosphorylated Src kinase and the amount of F-actin, and transiently the level of Tyr-phosphorylated ERK. Levels of total Src kinase, actin, GAP-43, cortactin and the glutamate receptor subunit GluN2B were not altered. When exposed to semaphorin-3a, Y-P30 protected a significant fraction of growth cones of cortical neurons from collapse. These results suggest that Y-P30 promotes axonal growth via Src- and ERK-dependent mechanisms which stabilize growth cones and confer resistance to collapsing factors. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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