Inhibition of Rho kinase (ROCK) increases neurite outgrowth on chondroitin sulphate proteoglycan in vitro and axonal regeneration in the adult optic nerve in vivo
2007 | Zeitschriftenartikel; Forschungsarbeit. Eine Publikation mit Affiliation zur Georg-August-Universität Göttingen.
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Zitiervorschlag
Inhibition of Rho kinase (ROCK) increases neurite outgrowth on chondroitin sulphate proteoglycan in vitro and axonal regeneration in the adult optic nerve in vivo
Lingor, P. ; Teusch, N.; Schwarz, K.; Mueller, R.; Mack, H.; Bähr, M. & Mueller, B. K. (2007)
Journal of Neurochemistry, 103(1) pp. 181-189. DOI: https://doi.org/10.1111/j.1471-4159.2007.04756.x
Dokumente & Medien
Details
- Autor(en)
- Lingor, P. ; Teusch, N.; Schwarz, K.; Mueller, R.; Mack, H.; Bähr, M. ; Mueller, B. K.
- Zusammenfassung
- Inhibitory molecules derived from CNS myelin and glial scar tissue are major causes for insufficient functional regeneration in the mammalian CNS. A multitude of these molecules signal through the Rho/Rho kinase (ROCK) pathway. We evaluated three inhibitors of ROCK, Y- 27632, Fasudil (HA-1077), and Dimethylfasudil (H-1152), in models of neurite outgrowth in vitro. We show, that all three ROCK inhibitors partially restore neurite outgrowth of Ntera-2 neurons on the inhibitory chondroitin sulphate proteoglycan substrate. In the rat optic nerve crush model Y-27632 dose-dependently increased regeneration of retinal ganglion cell axons in vivo. Application of Dimethylfasudil showed a trend towards increased axonal regeneration in an intermediate concentration. We demonstrate that inhibition of ROCK can be an effective therapeutic approach to increase regeneration of CNS neurons. The selection of a suitable inhibitor with a broad therapeutic window, however, is crucial in order to minimize unwanted side effects and to avoid deleterious effects on nerve fiber growth.
- Erscheinungsdatum
- 2007
- Zeitschrift
- Journal of Neurochemistry
- ISSN
- 0022-3042
- Sprache
- Englisch