Gliomas induce and exploit microglial MT1-MMP expression for tumor expansion

Research output: Contribution to journalJournal articleResearchpeer-review

  • D S Markovic
  • K Vinnakota
  • S Chirasani
  • M Synowitz
  • H Raguet
  • K Stock
  • M Sliwa
  • S Lehmann
  • R Kälin
  • N van Rooijen
  • Holmbeck, Kenn
  • F L Heppner
  • J Kiwit
  • V Matyash
  • S Lehnardt
  • B Kaminska
  • R Glass
  • H Kettenmann

Diffuse infiltration of glioma cells into normal brain tissue is considered to be a main reason for the unfavorable outcomes of patients with malignant gliomas. Invasion of glioma cells into the brain parenchyma is facilitated by metalloprotease-mediated degradation of the extracellular matrix. Metalloproteases are released as inactive pro-forms and get activated upon cleavage by membrane bound metalloproteases. Here, we show that membrane type 1 metalloprotease (MT1-MMP) is up-regulated in glioma-associated microglia, but not in the glioma cells. Overexpression of MT1-MMP is even lethal for glioma cells. Glioma-released factors trigger the expression and activity of MT1-MMP via microglial toll-like receptors and the p38 MAPK pathway, as deletion of the toll-like receptor adapter protein MyD88 or p38 inhibition prevented MT1-MMP expression and activity in cultured microglial cells. Microglial MT1-MMP in turn activates glioma-derived pro-MMP-2 and promotes glioma expansion, as shown in an ex vivo model using MT1-MMP-deficient brain tissue and a microglia depletion paradigm. Finally, MyD88 deficiency or microglia depletion largely attenuated glioma expansion in 2 independent in vivo models.

Original languageEnglish
JournalProceedings of the National Academy of Sciences of the United States of America
Volume106
Issue number30
Pages (from-to)12530-5
Number of pages6
ISSN0027-8424
DOIs
Publication statusPublished - 28 Jul 2009

    Research areas

  • Animals, Blotting, Western, Brain Neoplasms/genetics, Cell Line, Tumor, Enzyme Precursors/metabolism, Female, Gelatinases/metabolism, Gene Expression Regulation, Neoplastic, Glioma/genetics, Green Fluorescent Proteins/genetics, Humans, Immunohistochemistry, Male, Matrix Metalloproteinase 14/genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, Microglia/metabolism, Myeloid Differentiation Factor 88/genetics, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Toll-Like Receptors/metabolism, Tumor Burden, p38 Mitogen-Activated Protein Kinases/metabolism

ID: 201165473