Microglia Induce PDGFRB Expression in Glioma Cells to Enhance Their Migratory Capacity
High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is...
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| Published in | iScience Vol. 9; pp. 71 - 83 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier
30.11.2018
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| Subjects | |
| Online Access | Get full text |
| ISSN | 2589-0042 2589-0042 |
| DOI | 10.1016/j.isci.2018.10.011 |
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| Abstract | High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. |
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| AbstractList | High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB.High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. : Pathophysiology; Molecular Mechanism of Behavior; Immunology; Cancer Subject Areas: Pathophysiology, Molecular Mechanism of Behavior, Immunology, Cancer High-grade gliomas (HGGs) are the most aggressive and invasive primary brain tumors. The platelet-derived growth factor (PDGF) signaling pathway drives HGG progression, and enhanced expression of PDGF receptors (PDGFRs) is a well-established aberration in a subset of glioblastomas (GBMs). PDGFRA is expressed in glioma cells, whereas PDGFRB is mostly restricted to the glioma-associated stroma. Here we show that the spatial location of TAMMs correlates with the expansion of a subset of tumor cells that have acquired expression of PDGFRB in both mouse and human low-grade glioma and HCGs. Furthermore, M2-polarized microglia but not bone marrow (BM)-derived macrophages (BMDMs) induced PDGFRB expression in glioma cells and stimulated their migratory capacity. These findings illustrate a heterotypic cross-talk between microglia and glioma cells that may enhance the migratory and invasive capacity of the latter by inducing PDGFRB. • PDGFRB + glioma cells are in physical contact with IBA1 + TAMMs in mouse and human glioma • Aggregation of PDGFRB + glioma cells correlated with the accumulation of IBA1 + TAMMs • Microglia but not bone marrow-derived macrophages induced PDGFRB expression in vitro • M2-polarized microglia stimulated glioma cell migration dependent on PDGFRB Pathophysiology; Molecular Mechanism of Behavior; Immunology; Cancer |
| Author | Bolin, Sara Jiang, Yiwen Rolny, Charlotte Wallmann, Tatjana Andersson, John Bergh, Jonas Joly, Anne-Laure Harris, Robert A. Enger, Per Ø. Miletic, Hrvoje Wallerius, Majken Leiss, Lina Uhrbom, Lene Swartling, Fredrik J. Zhang, Xing-Mei Holland, Eric C. Sobocki, Caroline |
| AuthorAffiliation | 9 Division of Human Biology, Solid Tumor and Translational Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA 1 Karolinska Institutet, Department of Oncology-Pathology, CCK, R8:01, 171 76 Stockholm, Sweden 3 Uppsala University, Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, 751 85 Uppsala, Sweden 5 Neuro Clinic, Haukeland University Hospital, Bergen, Norway 7 Karolinska Institutet, Department of Medical Biochemistry and Biophysics, 17177 Stockholm, Sweden 10 Department of Neurosurgery, Haukeland University Hospital, Bergen, Norway 11 Department of Pathology, Haukeland University Hospital, Bergen, Norway 4 Karolinska Institutet, Department of Medicine, CMM, 171 76 Stockholm, Sweden 12 Department of Biomedicine, University of Bergen, Bergen, Norway 6 Oncomatrix Research Lab, University of Bergen, Bergen, Norway 2 Karolinska Institutet, Department of Clinical Neuroscience, Karolinska Hospital at Solna, CMM, 171 76 Stockholm, |
| AuthorAffiliation_xml | – name: 10 Department of Neurosurgery, Haukeland University Hospital, Bergen, Norway – name: 1 Karolinska Institutet, Department of Oncology-Pathology, CCK, R8:01, 171 76 Stockholm, Sweden – name: 12 Department of Biomedicine, University of Bergen, Bergen, Norway – name: 9 Division of Human Biology, Solid Tumor and Translational Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA – name: 11 Department of Pathology, Haukeland University Hospital, Bergen, Norway – name: 4 Karolinska Institutet, Department of Medicine, CMM, 171 76 Stockholm, Sweden – name: 6 Oncomatrix Research Lab, University of Bergen, Bergen, Norway – name: 7 Karolinska Institutet, Department of Medical Biochemistry and Biophysics, 17177 Stockholm, Sweden – name: 3 Uppsala University, Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, 751 85 Uppsala, Sweden – name: 5 Neuro Clinic, Haukeland University Hospital, Bergen, Norway – name: 8 Radiumhemmet, Karolinska University Hospital, 171 76 Stockholm, Sweden – name: 2 Karolinska Institutet, Department of Clinical Neuroscience, Karolinska Hospital at Solna, CMM, 171 76 Stockholm, Sweden |
| Author_xml | – sequence: 1 givenname: Tatjana surname: Wallmann fullname: Wallmann, Tatjana – sequence: 2 givenname: Xing-Mei surname: Zhang fullname: Zhang, Xing-Mei – sequence: 3 givenname: Majken surname: Wallerius fullname: Wallerius, Majken – sequence: 4 givenname: Sara surname: Bolin fullname: Bolin, Sara – sequence: 5 givenname: Anne-Laure surname: Joly fullname: Joly, Anne-Laure – sequence: 6 givenname: Caroline surname: Sobocki fullname: Sobocki, Caroline – sequence: 7 givenname: Lina surname: Leiss fullname: Leiss, Lina – sequence: 8 givenname: Yiwen surname: Jiang fullname: Jiang, Yiwen – sequence: 9 givenname: Jonas surname: Bergh fullname: Bergh, Jonas – sequence: 10 givenname: Eric C. surname: Holland fullname: Holland, Eric C. – sequence: 11 givenname: Per Ø. surname: Enger fullname: Enger, Per Ø. – sequence: 12 givenname: John surname: Andersson fullname: Andersson, John – sequence: 13 givenname: Fredrik J. surname: Swartling fullname: Swartling, Fredrik J. – sequence: 14 givenname: Hrvoje surname: Miletic fullname: Miletic, Hrvoje – sequence: 15 givenname: Lene surname: Uhrbom fullname: Uhrbom, Lene – sequence: 16 givenname: Robert A. surname: Harris fullname: Harris, Robert A. – sequence: 17 givenname: Charlotte surname: Rolny fullname: Rolny, Charlotte |
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