Age-dependent modulation of vascular niches for haematopoietic stem cells
Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic stem cell amplification. Age-linked changes in bone marrow Blood vessels in the bone marrow provide signals to the haematopoietic stem cells, ho...
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| Published in | Nature (London) Vol. 532; no. 7599; pp. 380 - 384 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
21.04.2016
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic stem cell amplification.
Age-linked changes in bone marrow
Blood vessels in the bone marrow provide signals to the haematopoietic stem cells, however, how these signals modulate haematopoietic stem cell (HSC) function and change as an organism age is unclear. Ralf Adams and colleagues used imaging and cell-type-specific genetic mouse models to investigate the nature of vascular niches for HSCs in bone. They find that Notch signalling in bone endothelial cells induces change in the capillaries and mesenchymal stem cells of the environment to support HSC amplification. These signals are reduced in aged organisms, but activation of Notch can restore some of these properties. Elsewhere in this issue (
page 323
), Tomer Itkin
et al
. show that the different functions of bone marrow endothelial cells are regulated by distinct types of endothelial blood vessels with different permeability properties, affecting levels of reactive oxygen species in their neighbouring stem cells.
Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells
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. 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-β (PDGFRβ)-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 PDGFRβ-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. |
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| AbstractList | 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-β (PDGFRβ)-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 PDGFRβ-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.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-β (PDGFRβ)-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 PDGFRβ-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. Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic stem cell amplification. Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic stem cell amplification. Age-linked changes in bone marrow Blood vessels in the bone marrow provide signals to the haematopoietic stem cells, however, how these signals modulate haematopoietic stem cell (HSC) function and change as an organism age is unclear. Ralf Adams and colleagues used imaging and cell-type-specific genetic mouse models to investigate the nature of vascular niches for HSCs in bone. They find that Notch signalling in bone endothelial cells induces change in the capillaries and mesenchymal stem cells of the environment to support HSC amplification. These signals are reduced in aged organisms, but activation of Notch can restore some of these properties. Elsewhere in this issue ( page 323 ), Tomer Itkin et al . show that the different functions of bone marrow endothelial cells are regulated by distinct types of endothelial blood vessels with different permeability properties, affecting levels of reactive oxygen species in their neighbouring stem cells. Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells 1 , 2 , 3 , 4 , 5 , 6 . 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-β (PDGFRβ)-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 PDGFRβ-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. Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells(1-6). The properties of nicheforming 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 (PDGFR beta)-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 PDGFR beta-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. Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells 1 – 6 . 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 PDGFRβ-positive perivascular cells, arteriole formation, and elevation of cellular stem cell factor levels. While endothelial hypoxia-inducible factor signalling promotes some of these aspects, it fails to enhance vascular niche function because of lacking arterialization and expansion of PDGFRβ-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 argue that vascular niches for haematopoietic stem cells are part of complex, age-dependent microenvironments involving multiple cell populations and vessel subtypes. Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells1-6. The properties of nicheforming 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-β (PDGFRβ)-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 PDGFRβ-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. Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic stem cell amplification. Age-linked changes in bone marrow Blood vessels in the bone marrow provide signals to the haematopoietic stem cells, however, how these signals modulate haematopoietic stem cell (HSC) function and change as an organism age is unclear. Ralf Adams and colleagues used imaging and cell-type-specific genetic mouse models to investigate the nature of vascular niches for HSCs in bone. They find that Notch signalling in bone endothelial cells induces change in the capillaries and mesenchymal stem cells of the environment to support HSC amplification. These signals are reduced in aged organisms, but activation of Notch can restore some of these properties. Elsewhere in this issue (( Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells.sup.1,2,3,4,5,6. 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] (PDGFR[beta])-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 PDGFR[beta]-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. 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-β (PDGFRβ)-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 PDGFRβ-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. |
| Audience | Academic |
| Author | Ramasamy, Saravana K. Langen, Urs H. Betsholtz, Christer Lapidot, Tsvee Kusumbe, Anjali P. Itkin, Tomer Mäe, Maarja Andaloussi Adams, Ralf H. |
| AuthorAffiliation | 3 Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden 2 Department of Immunology, The Weizmann Institute of Science, Rehovot , 76100, Israel 1 Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, D-48149 Münster, Germany 4 Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Scheeles väg 2, SE-171 77 Stockholm, Sweden |
| AuthorAffiliation_xml | – name: 3 Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, SE-751 85 Uppsala, Sweden – name: 2 Department of Immunology, The Weizmann Institute of Science, Rehovot , 76100, Israel – name: 4 Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Scheeles väg 2, SE-171 77 Stockholm, Sweden – name: 1 Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, D-48149 Münster, Germany |
| Author_xml | – sequence: 1 givenname: Anjali P. surname: Kusumbe fullname: Kusumbe, Anjali P. email: anjali.kusumbe@mpi-muenster.mpg.de organization: Department of Tissue Morphogenesis, Max-Planck-Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine – sequence: 2 givenname: Saravana K. surname: Ramasamy fullname: Ramasamy, Saravana K. organization: Department of Tissue Morphogenesis, Max-Planck-Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine – sequence: 3 givenname: Tomer surname: Itkin fullname: Itkin, Tomer organization: Department of Immunology, The Weizmann Institute of Science – sequence: 4 givenname: Maarja Andaloussi surname: Mäe fullname: Mäe, Maarja Andaloussi organization: Department of Immunology, Vascular Biology Program, Genetics and Pathology, Uppsala University – sequence: 5 givenname: Urs H. surname: Langen fullname: Langen, Urs H. organization: Department of Tissue Morphogenesis, Max-Planck-Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine – sequence: 6 givenname: Christer surname: Betsholtz fullname: Betsholtz, Christer organization: Department of Immunology, Vascular Biology Program, Genetics and Pathology, Uppsala University, Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute – sequence: 7 givenname: Tsvee surname: Lapidot fullname: Lapidot, Tsvee organization: Department of Immunology, The Weizmann Institute of Science – sequence: 8 givenname: Ralf H. surname: Adams fullname: Adams, Ralf H. email: ralf.adams@mpi-muenster.mpg.de organization: Department of Tissue Morphogenesis, Max-Planck-Institute for Molecular Biomedicine, and University of Münster, Faculty of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27074508$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-296853$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:133373900$$DView record from Swedish Publication Index |
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| Snippet | Notch signalling in endothelial cells of the bone induces change in the capillaries and mesenchymal stem cells of the environment to support haematopoietic... Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells. The... Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells1-6.... Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells 1 – 6... Blood vessels define local microenvironments in the skeletal system, play crucial roles in osteogenesis and provide niches for haematopoietic stem cells(1-6).... |
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| SubjectTerms | 631/136/16 631/532/1542 Aging Aging - physiology Animals Arterioles - cytology Arterioles - physiology Bone and Bones - blood supply Bone and Bones - cytology Bone and Bones - metabolism Bones Capillaries - cytology Capillaries - physiology Cell Count Cellular signal transduction Endothelial Cells - metabolism Endothelium Gene expression Growth Hematopoietic stem cells Hematopoietic Stem Cells - cytology Humanities and Social Sciences Hypoxia Hypoxia-Inducible Factor 1 - metabolism letter Ligands Male Mice Microenvironments multidisciplinary Observations Osteogenesis Physiological research Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Platelet-derived growth factor Properties Receptor, Platelet-Derived Growth Factor beta - metabolism Receptors, Notch - metabolism Science Signal Transduction Skeletal system Stem Cell Factor - metabolism Stem Cell Niche Stem cell research Stem cells Veins & arteries |
| Title | Age-dependent modulation of vascular niches for haematopoietic stem cells |
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