Bcl-x(L) increases axonal numbers but not axonal elongation from rat retinal explants.
The Bcl-2 family of proteins has been characterized as a key regulator of cell death programs. In addition, these proteins also play important roles in cellular differentiation, such as axonal growth. The role of Bcl-2 family members on axonal regeneration and neurite extension has been controversial so far. Here, we examine the influence of Bcl-x(L) on axonal regeneration from adult retina explants in vitro. We delivered recombinant Bcl-x(L) into retinal tissue, mediated by the Tat-protein transduction domain, and observed its effect on retinal axon extension. We found that Bcl-x(L) increased the number of regenerating neurites, but did not increase their length. Our results indicate that Bcl-x(L) stimulates axonal initiation but not axonal elongation after crush injury to retinal explants, without altering the number of surviving neurons.
Dietz
Gunnar P H
GP
DFG Research Center for Molecular Physiology of the Brain (CMPB), Neurologische Universitätsklinik, Waldweg 33, 37073 Göttingen, Germany. gdietz@gwdg.de
Dietz
Birgit
B
Bähr
Mathias
M
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology*; D002452:Cell Count; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects / Q000254:growth & development*; D051020:bcl-X Protein / Q000494:pharmacology / Q000502:physiology*
C494813:Bcl2l1 protein, rat; D051020:bcl-X Protein