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Microglia/macrophages and glioma progression
Author(s) -
Zhai Haiyan,
Gravanis Iordanis,
Tsirka Stella
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.568.15
Subject(s) - microglia , glioma , integrin alpha m , genetically modified mouse , u87 , cancer research , in vivo , medicine , transgene , pathology , biology , chemistry , immunology , immune system , inflammation , biochemistry , microbiology and biotechnology , gene
Gliomas are highly invasive brain tumors with the occurrence of numerous microglia/macrophages in and around the tumor. In this study, we used a glioma‐microglia co‐culture system to observe the details of their interactions. We generated a stable mouse glioma cell line GL261‐EGFP. When primary mouse microglia were treated with GL261‐conditioned medium, the expression of activation markers increased. When microglia were cultured with GL261‐EGFP, the phagocytic activity of microglia was inhibited. To study the contribution of microglia/macrophages to glioma progression in vivo, we used a mouse glioma model with microglia/macrophages ablation. CD11b‐HSVTK transgenic mice were used, which express herpes simplex thymidine kinase (HSVTK) in the cells of monocytic/microglial origin. Ganciclovir (GCV) was administered to the GL261‐EGFP injection site into the striatum. GCV was able to ablate microglia/macrophages in and around the tumor. This resulted in significant decrease in tumor sizes. The mice had much longer survival time as compared to the control group. These results suggest that glioma‐infiltrating microglia/macrophages can promote glioma growth, and that modulating their activity may be beneficial for glioma patients. Funding: NIH/NINDS R0142168