Biomedical Engineering Reference
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of stem cell delivered macrophage-microglial cells, and beta-1 integrin expression
might be enhancing factors of this angiogenic architecture over the ischemic brain.
Further studies are needed to prove this and other hypotheses.
In the recent work performed by Ratajczak and his group [ 20- 26 ] , with labeled
TCSCs and their mobilization into peripheral blood following stroke, the authors
hypothesized that the postnatal BM harbors a non-hematopoietic population of cells
that express markers on neural TCSCs that may account for the beneficial effects of
BM-derived cells in neural regeneration. These, neural TCSCs were chemoattracted
to the damaged neural tissue in an:
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SDF-1 −
-
CXCR4 −
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HGF-c-Met −
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LIF-LIF-R-dependent manner
These cells not only express neural lineage markers such as:
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Beta3-tubulin
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Nestin
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NeuN
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GFAPbut more importantly, form neurospheres in vitro. So, the BM has been
shown to contain a mobile pool of endothelial TCSCs that may play an important
role in organ regeneration.
Thus, the study was performed on B16, 129 wild-type mice and in vitro, for
neurosphere formation. The same group has also detected embryonic stem-cell
derived microvesicles that are selectively highly enriched in mRNA for several
pluripotent transcription factors as compared to parental ES [ 25 ] . These vesicles
suggest an evidence for horizontal transfer of mRNA and protein delivery to target
cells where they may be translated into the corresponding proteins [ 25 ] . The concept
that BM-derived cells participate in neural regeneration remains highly controver-
sial and the identity of the specific cell types involved remains unknown. The results
of Ratajczak's group (by using FACS analysis combined with analysis of neural
markers at the mRNA and protein levels) although still at the experimental level
revealed at least in mouse, the presence of this mobile cellular pool residing in non-
hematopoietic CXCR 4+/Sca − /lin − /CD45 − BM mononuclear cell fraction [ 26 ] .
Neural TCSC are mobilized into the peripheral blood during the stroke and chemoat-
tracted to the damaged neural tissue in a manner described above. Very recently, the
pool of VSELs and tissue committed progenitors was detected also in humans [ 26 ] .
Therefore, it would be worthwhile trying this product in clinical arena. In summary,
there is a potential for adult stem cells to regenerate damaged area in human brain
after the stroke, but the entire treatment has to be finely tuned with respect to type
and location of damage, and type of the cells that would be used. This apparently
involves optimal time and route of administration and optimizations of all conditions
in the patient that would allow for such approach.
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