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  • 1
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    Ephrin-B2 controls VEGF-induced angiogenesis and lymphangiogenesis (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-05-07
    Description: In development, tissue regeneration or certain diseases, angiogenic growth leads to the expansion of blood vessels and the lymphatic vasculature. This involves endothelial cell proliferation as well as angiogenic sprouting, in which a subset of cells, termed tip cells, acquires motile, invasive behaviour and extends filopodial protrusions. Although it is already appreciated that angiogenesis is triggered by tissue-derived signals, such as vascular endothelial growth factor (VEGF) family growth factors, the resulting signalling processes in endothelial cells are only partly understood. Here we show with genetic experiments in mouse and zebrafish that ephrin-B2, a transmembrane ligand for Eph receptor tyrosine kinases, promotes sprouting behaviour and motility in the angiogenic endothelium. We link this pro-angiogenic function to a crucial role of ephrin-B2 in the VEGF signalling pathway, which we have studied in detail for VEGFR3, the receptor for VEGF-C. In the absence of ephrin-B2, the internalization of VEGFR3 in cultured cells and mutant mice is defective, which compromises downstream signal transduction by the small GTPase Rac1, Akt and the mitogen-activated protein kinase Erk. Our results show that full VEGFR3 signalling is coupled to receptor internalization. Ephrin-B2 is a key regulator of this process and thereby controls angiogenic and lymphangiogenic growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yingdi -- Nakayama, Masanori -- Pitulescu, Mara E -- Schmidt, Tim S -- Bochenek, Magdalena L -- Sakakibara, Akira -- Adams, Susanne -- Davy, Alice -- Deutsch, Urban -- Luthi, Urs -- Barberis, Alcide -- Benjamin, Laura E -- Makinen, Taija -- Nobes, Catherine D -- Adams, Ralf H -- Cancer Research UK/United Kingdom -- England -- Nature. 2010 May 27;465(7297):483-6. doi: 10.1038/nature09002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Development Laboratory, Cancer Research UK London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20445537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Embryo Loss ; Embryo, Mammalian/blood supply/metabolism ; Endocytosis ; Endothelial Cells/cytology/metabolism ; Ephrin-B2/deficiency/genetics/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Humans ; *Lymphangiogenesis/genetics ; Lymphatic Vessels ; Mice ; Mice, Transgenic ; *Neovascularization, Physiologic/genetics ; Neuropeptides/metabolism ; Pregnancy ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, EphB4/deficiency/genetics/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor C/*metabolism ; Vascular Endothelial Growth Factor Receptor-3/metabolism ; Zebrafish ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Coupling of angiogenesis and osteogenesis by a specific vessel subtype in bone (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-22
    Description: The mammalian skeletal system harbours a hierarchical system of mesenchymal stem cells, osteoprogenitors and osteoblasts sustaining lifelong bone formation. Osteogenesis is indispensable for the homeostatic renewal of bone as well as regenerative fracture healing, but these processes frequently decline in ageing organisms, leading to loss of bone mass and increased fracture incidence. Evidence indicates that the growth of blood vessels in bone and osteogenesis are coupled, but relatively little is known about the underlying cellular and molecular mechanisms. Here we identify a new capillary subtype in the murine skeletal system with distinct morphological, molecular and functional properties. These vessels are found in specific locations, mediate growth of the bone vasculature, generate distinct metabolic and molecular microenvironments, maintain perivascular osteoprogenitors and couple angiogenesis to osteogenesis. The abundance of these vessels and associated osteoprogenitors was strongly reduced in bone from aged animals, and pharmacological reversal of this decline allowed the restoration of bone mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kusumbe, Anjali P -- Ramasamy, Saravana K -- Adams, Ralf H -- England -- Nature. 2014 Mar 20;507(7492):323-8. doi: 10.1038/nature13145. Epub 2014 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany [2]. ; 1] Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany [2] University of Munster, Faculty of Medicine, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24646994" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/metabolism/pathology ; Animals ; Blood Vessels/anatomy & histology/cytology/growth & development/*physiology ; Bone and Bones/*blood supply/cytology ; Endothelial Cells/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic/*physiology ; Osteoblasts/cytology/metabolism ; Osteogenesis/*physiology ; Oxygen/metabolism ; Stem Cells/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Endothelial Notch activity promotes angiogenesis and osteogenesis in bone (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-22
    Description: Blood vessel growth in the skeletal system and osteogenesis seem to be coupled, suggesting the existence of molecular crosstalk between endothelial and osteoblastic cells. Understanding the nature of the mechanisms linking angiogenesis and bone formation should be of great relevance for improved fracture healing or prevention of bone mass loss. Here we show that vascular growth in bone involves a specialized, tissue-specific form of angiogenesis. Notch signalling promotes endothelial cell proliferation and vessel growth in postnatal long bone, which is the opposite of the well-established function of Notch and its ligand Dll4 in the endothelium of other organs and tumours. Endothelial-cell-specific and inducible genetic disruption of Notch signalling in mice not only impaired bone vessel morphology and growth, but also led to reduced osteogenesis, shortening of long bones, chondrocyte defects, loss of trabeculae and decreased bone mass. On the basis of a series of genetic experiments, we conclude that skeletal defects in these mutants involved defective angiocrine release of Noggin from endothelial cells, which is positively regulated by Notch. Administration of recombinant Noggin, a secreted antagonist of bone morphogenetic proteins, restored bone growth and mineralization, chondrocyte maturation, the formation of trabeculae and osteoprogenitor numbers in endothelial-cell-specific Notch pathway mutants. These findings establish a molecular framework coupling angiogenesis, angiocrine signals and osteogenesis, which may prove significant for the development of future therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramasamy, Saravana K -- Kusumbe, Anjali P -- Wang, Lin -- Adams, Ralf H -- England -- Nature. 2014 Mar 20;507(7492):376-80. doi: 10.1038/nature13146. Epub 2014 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany [2]. ; Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany. ; 1] Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany [2] University of Munster, Faculty of Medicine, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24647000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Blood Vessels/growth & development ; Bone Development/drug effects ; Bone and Bones/*blood supply/cytology/drug effects/*metabolism ; Calcification, Physiologic/drug effects ; Carrier Proteins/administration & dosage/metabolism/pharmacology ; Cell Proliferation ; Chondrocytes/cytology/drug effects ; Endothelium, Vascular/cytology/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; *Neovascularization, Physiologic ; *Osteogenesis/drug effects ; Receptors, Notch/*metabolism ; Signal Transduction/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-20
    Description: Developing tissues and growing tumours produce vascular endothelial growth factors (VEGFs), leading to the activation of the corresponding receptors in endothelial cells. The resultant angiogenic expansion of the local vasculature can promote physiological and pathological growth processes. Previous work has uncovered that the VEGF and Notch pathways are tightly linked. Signalling triggered by VEGF-A (also known as VEGF) has been shown to induce expression of the Notch ligand DLL4 in angiogenic vessels and, most prominently, in the tip of endothelial sprouts. DLL4 activates Notch in adjacent cells, which suppresses the expression of VEGF receptors and thereby restrains endothelial sprouting and proliferation. Here we show, by using inducible loss-of-function genetics in combination with inhibitors in vivo, that DLL4 protein expression in retinal tip cells is only weakly modulated by VEGFR2 signalling. Surprisingly, Notch inhibition also had no significant impact on VEGFR2 expression and induced deregulated endothelial sprouting and proliferation even in the absence of VEGFR2, which is the most important VEGF-A receptor and is considered to be indispensable for these processes. By contrast, VEGFR3, the main receptor for VEGF-C, was strongly modulated by Notch. VEGFR3 kinase-activity inhibitors but not ligand-blocking antibodies suppressed the sprouting of endothelial cells that had low Notch signalling activity. Our results establish that VEGFR2 and VEGFR3 are regulated in a highly differential manner by Notch. We propose that successful anti-angiogenic targeting of these receptors and their ligands will strongly depend on the status of endothelial Notch signalling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benedito, Rui -- Rocha, Susana F -- Woeste, Marina -- Zamykal, Martin -- Radtke, Freddy -- Casanovas, Oriol -- Duarte, Antonio -- Pytowski, Bronislaw -- Adams, Ralf H -- England -- Nature. 2012 Mar 18;484(7392):110-4. doi: 10.1038/nature10908.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, D-48149 Munster, Germany. rui.benedito@mpi-muenster.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22426001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Endothelial Cells/cytology/drug effects/metabolism ; Female ; HEK293 Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; Intracellular Signaling Peptides and Proteins/deficiency/genetics/metabolism ; Male ; Membrane Proteins/deficiency/genetics/metabolism ; Mice ; Models, Biological ; Neovascularization, Physiologic/drug effects/*physiology ; Protein Kinase Inhibitors/pharmacology ; Receptors, Notch/antagonists & inhibitors/*metabolism ; *Signal Transduction/drug effects ; Transcription, Genetic ; *Up-Regulation ; Vascular Endothelial Growth Factor A/*metabolism ; Vascular Endothelial Growth Factor Receptor-2/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor Receptor-3/biosynthesis/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Expression and function of junctional adhesion molecule-C in myelinated peripheral nerves (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: JAM-C is an adhesion molecule that is expressed on cells within the vascular compartment and epithelial cells and, to date, has been largely studied in the context of inflammatory events. Using immunolabeling procedures in conjunction with confocal and electron microscopy, we show here that JAM-C is also expressed in peripheral nerves and that this expression is localized to Schwann cells at junctions between adjoining myelin end loops. Sciatic nerves from JAM-C-deficient [having the JAM-C gene knocked out (KO)] mice exhibited loss of integrity of the myelin sheath and defective nerve conduction as indicated by morphological and electrophysiological studies, respectively. In addition, behavioral tests showed motor abnormalities in the KO animals. JAM-C was also expressed in human sural nerves with an expression profile similar to that seen in mice. These results demonstrate that JAM-C is a component of the autotypic junctional attachments of Schwann cells and plays an important role in maintaining the integrity and function of myelinated peripheral nerves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299566/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299566/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheiermann, Christoph -- Meda, Paolo -- Aurrand-Lions, Michel -- Madani, Rime -- Yiangou, Yiangos -- Coffey, Peter -- Salt, Thomas E -- Ducrest-Gay, Dominique -- Caille, Dorothee -- Howell, Owain -- Reynolds, Richard -- Lobrinus, Alexander -- Adams, Ralf H -- Yu, Alan S L -- Anand, Praveen -- Imhof, Beat A -- Nourshargh, Sussan -- 064920/Wellcome Trust/United Kingdom -- PG/03/123/16102/British Heart Foundation/United Kingdom -- R01 DK062283/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1472-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart and Lung Institute, Imperial College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048693" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Adhesion Molecules/*metabolism ; Humans ; Immunoglobulins/*metabolism ; Intercellular Junctions/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Knockout ; Myelin Sheath/metabolism/*physiology/ultrastructure ; Nerve Fibers, Myelinated/metabolism/*physiology/ultrastructure ; Neural Conduction ; Peripheral Nerves/*metabolism/physiology ; Peripheral Nervous System Diseases/metabolism/pathology/physiopathology ; Schwann Cells/*metabolism ; Sciatic Nerve/metabolism/physiology/ultrastructure ; Sural Nerve/metabolism/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Development. Aorta's cardinal secret (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benedito, Rui -- Adams, Ralf H -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):242-3. doi: 10.1126/science.1181033.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, 48149 Munster, Germany, and Faculty of Medicine, University of Munster, 48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/*embryology ; Arteries/cytology/*embryology ; Blood Circulation ; Cell Movement ; Endothelial Cells/cytology/metabolism/*physiology ; Ephrin-B2/metabolism ; Lymphatic Vessels/embryology ; Mice ; *Morphogenesis ; Neovascularization, Physiologic ; Receptor, EphB4/metabolism ; Signal Transduction ; Stem Cells/cytology/physiology ; Veins/cytology/*embryology ; Zebrafish ; Zebrafish Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Distinct bone marrow blood vessels differentially regulate haematopoiesis (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-04-14
    Description: Bone marrow endothelial cells (BMECs) form a network of blood vessels that regulate both leukocyte trafficking and haematopoietic stem and progenitor cell (HSPC) maintenance. However, it is not clear how BMECs balance these dual roles, and whether these events occur at the same vascular site. We found that mammalian bone marrow stem cell maintenance and leukocyte trafficking are regulated by distinct blood vessel types with different permeability properties. Less permeable arterial blood vessels maintain haematopoietic stem cells in a low reactive oxygen species (ROS) state, whereas the more permeable sinusoids promote HSPC activation and are the exclusive site for immature and mature leukocyte trafficking to and from the bone marrow. A functional consequence of high permeability of blood vessels is that exposure to blood plasma increases bone marrow HSPC ROS levels, augmenting their migration and differentiation, while compromising their long-term repopulation and survival. These findings may have relevance for clinical haematopoietic stem cell transplantation and mobilization protocols.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Itkin, Tomer -- Gur-Cohen, Shiri -- Spencer, Joel A -- Schajnovitz, Amir -- Ramasamy, Saravana K -- Kusumbe, Anjali P -- Ledergor, Guy -- Jung, Yookyung -- Milo, Idan -- Poulos, Michael G -- Kalinkovich, Alexander -- Ludin, Aya -- Kollet, Orit -- Shakhar, Guy -- Butler, Jason M -- Rafii, Shahin -- Adams, Ralf H -- Scadden, David T -- Lin, Charles P -- Lapidot, Tsvee -- EB017274/EB/NIBIB NIH HHS/ -- HL100402/HL/NHLBI NIH HHS/ -- R01 EB017274/EB/NIBIB NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):323-8. doi: 10.1038/nature17624. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. ; Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Harvard Stem Cell Institute, Cambridge, Massachusetts 02114, USA. ; Center for Regenerative Medicine and Cancer Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. ; Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and Faculty of Medicine, University of Munster, D-48149 Munster, Germany. ; Internal Medicine Department, Tel-Aviv Sourasky Medical Center, Tel-Aviv 64239, Israel. ; Department of Genetic Medicine, Weill Cornell Medical College, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/metabolism ; Arteries/cytology/physiology ; Blood Vessels/*cytology/*physiology ; Bone Marrow/*blood supply ; Bone Marrow Cells/cytology ; Cell Differentiation ; Cell Movement ; Cell Self Renewal ; Cell Survival ; Chemokine CXCL12/metabolism ; Endothelial Cells/physiology ; Female ; *Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Leukocytes/cytology ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Nestin/metabolism ; Pericytes/physiology ; Permeability ; Plasma/metabolism ; Reactive Oxygen Species/metabolism ; Receptors, CXCR4/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Age-dependent modulation of vascular niches for haematopoietic stem cells (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-04-14
    Description: Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells. The properties of niche-forming vessels and their changes in the ageing organism remain incompletely understood. Here we show that Notch signalling in endothelial cells leads to the expansion of haematopoietic stem cell niches in bone, which involves increases in CD31-positive capillaries and platelet-derived growth factor receptor-beta (PDGFRbeta)-positive perivascular cells, arteriole formation and elevated levels of cellular stem cell factor. Although endothelial hypoxia-inducible factor signalling promotes some of these changes, it fails to enhance vascular niche function because of a lack of arterialization and expansion of PDGFRbeta-positive cells. In ageing mice, niche-forming vessels in the skeletal system are strongly reduced but can be restored by activation of endothelial Notch signalling. These findings indicate that vascular niches for haematopoietic stem cells are part of complex, age-dependent microenvironments involving multiple cell populations and vessel subtypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kusumbe, Anjali P -- Ramasamy, Saravana K -- Itkin, Tomer -- Mae, Maarja Andaloussi -- Langen, Urs H -- Betsholtz, Christer -- Lapidot, Tsvee -- Adams, Ralf H -- England -- Nature. 2016 Apr 21;532(7599):380-4. doi: 10.1038/nature17638. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Munster, Faculty of Medicine, D-48149 Munster, Germany. ; Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. ; Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden. ; Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Scheeles vag 2, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074508" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Antigens, CD31/metabolism ; Arterioles/cytology/*physiology ; Bone and Bones/*blood supply/cytology/metabolism ; Capillaries/cytology/*physiology ; Cell Count ; Endothelial Cells/metabolism ; Hematopoietic Stem Cells/*cytology ; Hypoxia-Inducible Factor 1/metabolism ; Male ; Mice ; Osteogenesis ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Stem Cell Factor/metabolism ; *Stem Cell Niche
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    The endothelial transcription factor ERG mediates Angiopoietin-1-dependent control of Notch signalling and vascular stability (2017)
    Springer Nature
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    Publication Date: 2017-07-12
    Description: The endothelial transcription factor ERG mediates Angiopoietin-1-dependent control of Notch signalling and vascular stability Nature Communications, Published online: 11 July 2017; doi:10.1038/ncomms16002 Vascular maturation and stability is regulated by Notch and Angiopoietin-1/Tie2 signalling. Here, Shah et al . show that the transcription factor ERG coordinates the Ang1, Notch and Wnt/β-catenin pathways to promote vascular maturation and stability.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 10
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    Development and Reservoir Analysis of Momotombo Geothermal Project, Nicaragua: ABSTRACT (1978)
    American Association of Petroleum Geologists
    Details
    Publication Date: 1978-01-01
    Print ISSN: 0149-1423
    Electronic ISSN: 1943-2674
    Topics: Geosciences
    Published by American Association of Petroleum Geologists
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