Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/45516
Título: Tenascin-R and axon growth-promoting molecules are up-regulated in the regenerating visual pathway of the lizard (Gallotia galloti)
Autores/as: Lang, Dirk M.
Monzon-Mayor, Maximina 
Romero-Aleman, Maria Del Mar 
Yanes, Carmen 
Santos, Elena
Pesheva, Penka
Palabras clave: Optic-Nerve Regeneration
Chondroitin Sulfate Proteoglycan
Repellent Guidance Molecule
Retinal Ganglion-Cells
Spinal-Cord-Injury, et al.
Fecha de publicación: 2008
Editor/a: 1932-8451
Publicación seriada: Developmental Neurobiology 
Resumen: It is currently unclear whether retinal ganglion cell (RGC) axon regeneration depends on down-regulation of axon growth-inhibitory proteins, and to what extent outgrowth-promoting substrates contribute to RGC axon regeneration in reptiles. We performed an immunohistochemical study of the regulation of the axon growth-inhibiting extracellular matrix molecules tenascin-R and chondroitin sulphate proteoglycan (CSPG), the axon outgrowth-promoting extracellular matrix proteins fibronectin and laminin, and the axonal tenascin-R receptor protein F3/contactin during RGC axon regeneration in the lizard, Gallotia galloti. Tenascin-R and CSPG were expressed in an extracellular matrix-, oligodendrocyte/myelin- and neuron-associated pattern and up-regulated in the regenerating optic pathway. The expression pattern of tenascin-R was not indicative of a role in channeling or restriction of re-growing RGC axons. Up-regulation of fibronectin, laminin, and F3/contactin occurred in spatiotemporal patterns corresponding to tenascin-R expression. Moreover, we analyzed the influence of substrates containing tenascin-R, fibronectin, and laminin on outgrowth of regenerating lizard RGC axons. In vitro regeneration of RGC axons was not inhibited by tenascin-R, and further improved on mixed substrates containing tenascin-R together with fibronectin or laminin. These results indicate that RGC axon regeneration in Gallotia galloti does not require down-regulation of tenascin-R or CSPG. Presence of tenascin-R is insufficient to prevent RGC axon growth, and concomitant up-regulation of axon growth-promoting molecules like fibronectin and laminin may override the effects of neurite growth inhibitors on RGC axon regeneration. Up-regulation of contactin in RGCs suggests that tenascin-R may have an instructive function during axon regeneration in the lizard optic pathway. (C) 2008 Wiley Periodicals, Inc.
URI: http://hdl.handle.net/10553/45516
ISSN: 1932-8451
DOI: 10.1002/dneu.20624
Fuente: Developmental Neurobiology[ISSN 1932-8451],v. 68, p. 899-916
Colección:Artículos
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