Title: Overexpression of a truncated TrkB isoform increases the proliferation of neural progenitors
Authors: Tervonen, Topi A
Ajamian, Farzam
de Wit, Joris
Verhaagen, Joost
Castren, Eero
Castren, Maija # ×
Issue Date: Sep-2006
Publisher: Published on behalf of the European Neuroscience Association by Oxford University Press
Series Title: European Journal of Neuroscience vol:24 issue:5 pages:1277-1285
Abstract: Abstract
The truncated isoform of TrkB, TrkB.T1, has been shown to be expressed in the neurogenic region of rodent brain. TrkB.T1 lacks
tyrosine kinase activity and it may modify the action of the full-length TrkB. We show here that the full-length TrkB and TrkB.T1 are
expressed at the same relative expression levels in mouse neural progenitor cell cultures. The number of neurosphere-forming
progenitors was reduced and apoptosis increased in neurospheres generated from mice overexpressing TrkB.T1 when compared
with wild-type neurospheres. The proliferation of the transgenic neural progenitors was increased, as indicated by the larger average
diameter of spheres (140% of control), the increased cell growth in an MTT assay (137% of control) and the faster rate of
3H-thymidine incorporation (128% of control) in the transgenic cell cultures than in controls. The proliferation of neural progenitors
was also increased after lentivirus-mediated TrkB.T1 overexpression. A significant increase in 3H-thymidine incorporation (119% of
control) and the average diameter of spheres (112% of control) in the TrkB.T1-transduced neurospheres compared with
neurospheres transduced with the control vectors confirmed the role of TrkB.T1 in proliferation of neural progenitor. When induced to
differentiate, progenitors overexpressing TrkB.T1 generated two to three times more neurons than did wild-type cells. The increase in
the number of neurons correlated with an increase in the number of apoptotic cells (two-fold) at these time points. The data indicate
that changes in the relative expression levels of different TrkB isoforms influence the replicative capacity of neural progenitors.
ISSN: 0953-816X
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Non-KU Leuven Association publications
× corresponding author
# (joint) last author

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