Differentiation of vascular smooth muscle cells from local precursors during embryonic and adult arteriogenesis requires Notch signaling

Vascular smooth muscle cells (VSMC) have been suggested to arise from various developmental sources during embryogenesis, depending on the vascular bed. However, evidence also points to a common subpopulation of vascular progenitor cells predisposed to VSMC fate in the embryo. In the present study,...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2012-05, Vol.109 (18), p.6993-6998
Main Authors: Chang, Linda, Noseda, Michela, Higginson, Michelle, Ly, Michelle, Patenaude, Alexandre, Fuller, Megan, Kyle, Alastair H, Minchinton, Andrew I, Puri, Mira C, Dumont, Daniel J, Karsan, Aly
Format: Article
Language:English
Subjects:
adults
Animals
Antigens, CD - genetics
Aorta
Arteries
Arteries - embryology
Arteries - growth & development
Arteries - metabolism
Base Sequence
Biological Sciences
Cadherins - deficiency
Cadherins - genetics
Cell Differentiation - genetics
Cell Differentiation - physiology
Cell lines
Cells
DNA Primers - genetics
embryogenesis
Embryonic cells
Embryonic stem cells
Embryos
Endothelial cells
Female
Hematopoietic stem cells
hemorrhage
Leukocyte Common Antigens - deficiency
Leukocyte Common Antigens - genetics
Mesenchymal stem cells
Mice
Mice, Transgenic
Myoblasts, Smooth Muscle - cytology
Myoblasts, Smooth Muscle - metabolism
myocytes
Myocytes, Smooth Muscle - cytology
Myocytes, Smooth Muscle - metabolism
Neovascularization, Physiologic - genetics
Platelet Endothelial Cell Adhesion Molecule-1 - metabolism
Pregnancy
Proteins
Receptor, TIE-1 - metabolism
Receptors, Notch - antagonists & inhibitors
Receptors, Notch - metabolism
Rodents
Signal Transduction
Smooth muscle
Smooth muscle myocytes
stem cells
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Summary:Vascular smooth muscle cells (VSMC) have been suggested to arise from various developmental sources during embryogenesis, depending on the vascular bed. However, evidence also points to a common subpopulation of vascular progenitor cells predisposed to VSMC fate in the embryo. In the present study, we use binary transgenic reporter mice to identify a Tie1+CD31dimvascular endothelial (VE)-cadherin–CD45– precursor that gives rise to VSMC in vivo in all vascular beds examined. This precursor does not represent a mature endothelial cell, because a VE-cadherin promoter-driven reporter shows no expression in VSMC during murine development. Blockade of Notch signaling in the Tie1+ precursor cell, but not the VE-cadherin+ endothelial cell, decreases VSMC investment of developing arteries, leading to localized hemorrhage in the embryo at the time of vascular maturation. However, Notch signaling is not required in the Tie1+ precursor after establishment of a stable artery. Thus, Notch activity is required in the differentiation of a Tie1+ local precursor to VSMC in a spatiotemporal fashion across all vascular beds.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1118512109