TAL1/SCL transcription factor in vascular processes

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TAL1/SCL transcription factor in vascular processes

Postby patoco » Wed Sep 20, 2006 8:32 pm

Expression of the TAL1/SCL transcription factor in physiological and pathological vascular processes.

July 14, 2006

Tang T, Shi Y, Opalenik SR, Brantley-Sieders DM, Chen J, Davidson JM,
Brandt SJ.

Department of Medicine, Vanderbilt University Medical Center,
Nashville, TN 37232, USA.

The TAL1/SCL transcription factor is essential for haematopoietic
commitment and vascular remodelling during embryonic development. To
help clarify its role in postnatal vascular processes, we characterized
the expression of mouse Tal1 protein by immunocytochemistry in several
experimental models of blood vessel formation. In adult mice, Tal1
protein was expressed in rare microvascular endothelial cells and in
extravascular cells provisionally identified as endothelial progenitors
from their morphology, proximity to vessels and expression of vascular
endothelial growth factor receptor-2. The number of Tal1-expressing
endothelial cells increased significantly but transiently in all the
models-hormone-induced ovulation, wound healing and tumour development.

Finally, Tal1 protein was detected in the nuclei of newly formed
lymphatic endothelial cells in tumour-bearing animals. These results
show that TAL1 is expressed by vascular endothelial cells and
endothelial progenitors at sites of physiological and pathological
neovascularization and suggest a role for this transcription factor in
adult vasculogenesis. This work also provides the first evidence for
TAL1 expression in lymphangiogenesis. Copyright (c) 2006 Pathological
Society of Great Britain and Ireland. Published by John Wiley & Sons,

PMID: 16841371 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16841371


Related studies on TAL1/SCL:


Lmo2 and Scl/Tal1 convert non-axial mesoderm into haemangioblasts which differentiate into endothelial cells in the absence of Gata1



Phosphorylation by mitogen-activated protein kinase mediates the hypoxia-induced turnover of the TAL1/SCL transcription factor in endothelial cells.



Combinatorial effects of Flk1 and Tal1 on vascular and hematopoietic development in the mouse.

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