HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Microglia Induce PDGFRB Expression in Glioma Cells to Enhance Their Migratory Capacity.

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.
AuthorsTatjana Wallmann, Xing-Mei Zhang, Majken Wallerius, Sara Bolin, Anne-Laure Joly, Caroline Sobocki, Lina Leiss, Yiwen Jiang, Jonas Bergh, Eric C Holland, Per Ø Enger, John Andersson, Fredrik J Swartling, Hrvoje Miletic, Lene Uhrbom, Robert A Harris, Charlotte Rolny
JournaliScience (iScience) Vol. 9 Pg. 71-83 (Nov 30 2018) ISSN: 2589-0042 [Electronic] United States
PMID30384135 (Publication Type: Journal Article)
CopyrightCopyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: