Leukaemia
Parkinson
Anticancer
Res. 2006 Jan-Feb;26(1B):543-7. Stem Cells.
2006 Jun 1; [Epub ahead of print]
Plasma CD105,
TGFbeta-1, TGFbeta-3 and the ligand/receptor
complexes in children with acute lymphoblastic leukaemia.
Al-Mowallad A, Carr
T, Al-Qouzi A, Li
C, Byers
R, Kumar
S.
Division of Laboratory and Regenerative Medicine, The
University of
The role of angiogenesis in solid tumours is well
recognised, but its importance in haematological malignancies is less well understood. In
leukaemia, mainly the determination of microvascular density utilising
immunohistochemistry in the bone marrow trephines
and the measurement of soluble angiogenic factors
have led to the recognition that angiogenesis may be important in leukaemia as well. In this study, the soluble form of
the endothelial cell activation/proliferation (i.e., angiogenesis) marker
CD105 and its ligands TGFbeta-1 and -3, as well
as the ligand/receptor complexes in plasma from
children with acute lymphoblastic leukaemia (ALL) were quantified. The plasma level of
CD105 was significantly higher in patients with common ALL compared to
controls, while the TGFbeta-3 level was lower in patients. Neither the
CD105 or TGFbeta-3 levels were of prognostic value, nor did they correlate
with any of the known prognostic indicators, such as white blood cell
counts. There were no significant differences between the plasma levels of
any of the other parameters, such as TGFbeta-1 or the ligand
receptor complexes, in children with leukaemia
compared to controls. Our results support the role of angiogenesis in leukaemia and suggest that anti-angiogenesis may be a
therapeutic target in leukaemia.
PMID: 16739317 [PubMed - indexed for MEDLINE
TGF-{beta} is required for
differentiation of mouse mesencephalic
progenitors into dopaminergic neurons in vitro
and in vivo. Ectopic induction in dorsal mesencephalon.
Roussa E, Wiehle M, Dunker
N, Becker-Katins S, Oehlke O, Krieglstein K.
Georg-August-University
Gottingen,
Tissue engineering is a prerequisite for cell replacement as therapeutic
strategy for degenerative diseases, such as Parkinson's disease. In the present
study, we investigate regional identity of mesencephalic
neural progenitors and characterize their development towards ventral mesencephalic dopaminergic
neurons. We show that neural progenitors from ventral and dorsal mouse E12 mesencephalon exhibit regional identity in vitro.
Treatment of ventral midbrain dissociated neurospheres
with TGF-beta increased the number of Nurr1 and TH immunoreactive
cells, which can be further increased when the spheres were treated with
TGF-beta in combination with Shh and FGF8.
TGF-beta differentiation signaling is TGF-beta receptor-mediated, involving
the Smad as well as the p38 MAPK pathway. In
vivo, TGF-beta2/-beta3 double knockout mice embryos revealed significantly
reduced numbers of TH labeled cells in ventral mesencephalon,
but not in locus coeruleus. TH reduction in Tgfbeta2(-/-)/Tgfbeta3(+/-) was higher than in
Tgf-beta2(+/-)/Tgf-beta3(-/-). Most importantly, TGF-beta may ectopically
induce TH immunopositive cells in dorsal mesencephalon in vitro, in a Shh-
and FGF8- independent manner. Together, the results clearly demonstrate
TGF-beta2 and TGF-beta3 as essential signals for differentiation of
midbrain progenitors towards neuronal fate and dopaminergic
phenotype.
PMID: 16741229 [PubMed - as supplied by publisher]