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Content Provider | World Health Organization (WHO)-Global Index Medicus |
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Author | Cristofaro, Brunella Shi, Yu Faria, Marcella Suchting, Steven Leroyer, Aurelie S. Trindade, Alexandre Duarte, Antonio Zovein, Ann C. Iruela-Arispe, M. Luisa Nih, Lina R. Kubis, Nathalie Henrion, Daniel Loufrani, Laurent Todiras, Mihail Schleifenbaum, Johanna Gollasch, Maik Zhuang, Zhen W. Simons, Michael Eichmann, Anne Le Noble, Ferdinand |
Description | Country affiliation: France Author Affiliation: Cristofaro B ( CIRB Collège de France, Inserm U1050/CNRS UMR 7241, Paris, France.) |
Abstract | Arteriogenesis requires growth of pre-existing arteriolar collateral networks and determines clinical outcome in arterial occlusive diseases. Factors responsible for the development of arteriolar collateral networks are poorly understood. The Notch ligand Delta-like 4 (Dll4) promotes arterial differentiation and restricts vessel branching. We hypothesized that Dll4 may act as a genetic determinant of collateral arterial networks and functional recovery in stroke and hind limb ischemia models in mice. Genetic loss- and gain-of-function approaches in mice showed that Dll4-Notch signaling restricts pial collateral artery formation by modulating arterial branching morphogenesis during embryogenesis. Adult Dll4(+/-) mice showed increased pial collateral numbers, but stroke volume upon middle cerebral artery occlusion was not reduced compared with wild-type littermates. Likewise, Dll4(+/-) mice showed reduced blood flow conductance after femoral artery occlusion, and, despite markedly increased angiogenesis, tissue ischemia was more severe. In peripheral arteries, loss of Dll4 adversely affected excitation-contraction coupling in arterial smooth muscle in response to vasopressor agents and arterial vessel wall adaption in response to increases in blood flow, collectively contributing to reduced flow reserve. We conclude that Dll4-Notch signaling modulates native collateral formation by acting on vascular branching morphogenesis during embryogenesis. Dll4 furthermore affects tissue perfusion by acting on arterial function and structure. Loss of Dll4 stimulates collateral formation and angiogenesis, but in the context of ischemic diseases such beneficial effects are overruled by adverse functional changes, demonstrating that ischemic recovery is not solely determined by collateral number but rather by vessel functionality. |
File Format | HTM / HTML |
ISSN | 09501991 |
e-ISSN | 14779129 |
DOI | 10.1242/dev.092304 |
Journal | Development |
Issue Number | 8 |
Volume Number | 140 |
Language | English |
Publisher | The Company of Biologists |
Publisher Date | 2013-04-01 |
Publisher Place | Great Britain (UK) |
Access Restriction | Open |
Subject Keyword | Discipline Developmental Discipline Biology Intracellular Signaling Peptides And Proteins Metabolism Ischemia Physiopathology Membrane Proteins Microvessels Embryology Morphogenesis Physiology Neovascularization, Physiologic Receptors, Notch Signal Transduction Analysis Of Variance Animals Immunohistochemistry Mice Real-time Polymerase Chain Reaction Regional Blood Flow X-ray Microtomography Research Support, Non-u.s. Gov't |
Content Type | Text |
Resource Type | Article |
Subject | Developmental Biology Molecular Biology |
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