GDNF mediates glioblastoma-induced microglia attraction but not astrogliosis
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Updated: May 14, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
Min-Chi Ku1, Susanne A Wolf, Dorota Respondek
1Department of Cellular Neuroscience, Max Delbrück Center for Molecular Medicine (MDC), Robert Rössle Str. 10, 13125 Berlin, Germany.
Abstract:
High-grade gliomas are the most common primary brain tumors. Their malignancy is promoted by the complex crosstalk between different cell types in the central nervous system. Microglia/brain macrophages infiltrate high-grade gliomas and contribute to their progression. To identify factors that mediate the attraction of microglia/macrophages to malignant brain tumors, we established a glioma cell encapsulation model that was applied in vivo. Mouse GL261 glioma cell line and human high-grade glioma cells were seeded into hollow fibers (HF) that allow the passage of soluble molecules but not cells. The glioma cell containing HF were implanted into one brain hemisphere and simultaneously HF with non-transformed fibroblasts (controls) were introduced into the contralateral hemisphere. Implanted mouse and human glioma- but not fibroblast-containing HF attracted microglia and up-regulated immunoreactivity for GFAP, which is a marker of astrogliosis. In this study, we identified GDNF as an important factor for microglial attraction: (1) GL261 and human glioma cells secret GDNF, (2) reduced GDNF production by siRNA in GL261 in mouse glioma cells diminished attraction of microglia, (3) over-expression of GDNF in fibroblasts promoted microglia attraction in our HF assay. In vitro migration assays also showed that GDNF is a strong chemoattractant for microglia. While GDNF release from human or mouse glioma had a profound effect on microglial attraction, the glioma-induced astrogliosis was not affected. Finally, we could show that injection of GL261 mouse glioma cells with GDNF knockdown by shRNA into mouse brains resulted in reduced tumor expansion and improved survival as compared to injection of control cells.
Insights
Glial cell-derived neurotrophic factor (GDNF) attracts microglia to brain tumors. Reducing GDNF in glioma cells slowed tumor growth and improved survival in mice, highlighting GDNF as a therapeutic target.
Area of Science:
- Neuro-oncology
- Cancer immunology
- Cellular biology
Background:
- High-grade gliomas are aggressive brain tumors driven by cellular interactions.
- Microglia and brain macrophages infiltrate gliomas, promoting tumor progression.
- Understanding factors attracting these immune cells is crucial for therapeutic strategies.
Purpose of the Study:
- To identify key factors mediating microglial/macrophage attraction to high-grade gliomas.
- To investigate the role of Glial cell-derived neurotrophic factor (GDNF) in this process.
- To evaluate the therapeutic potential of targeting GDNF in glioma treatment.
Main Methods:
- Development of an in vivo glioma cell encapsulation model using hollow fibers (HF).
- Implantation of HF containing human or mouse glioma cells versus control fibroblasts into mouse brains.
- Assessment of microglial attraction, astrogliosis (GFAP), and GDNF levels.
- Genetic manipulation (siRNA, shRNA, overexpression) of GDNF in glioma cells and fibroblasts.
- In vitro microglial migration assays and in vivo tumor growth studies.
Main Results:
- Glioma-containing HF, but not fibroblast HF, attracted microglia and induced astrogliosis.
- GDNF was identified as a critical chemoattractant, secreted by glioma cells.
- Reduced GDNF levels diminished microglial attraction, while GDNF overexpression enhanced it.
- GDNF significantly attracted microglia in vitro; glioma-induced astrogliosis was unaffected.
- GDNF knockdown in glioma cells reduced tumor expansion and improved mouse survival.
Conclusions:
- GDNF is a key mediator of microglial attraction to high-grade gliomas.
- Targeting GDNF may represent a novel therapeutic strategy for reducing glioma progression.
- Further research into GDNF's role in the tumor microenvironment is warranted.
