Microglia/macrophages promote glioma progression.

نویسندگان

  • Haiyan Zhai
  • Frank L Heppner
  • Stella E Tsirka
چکیده

Gliomas are highly aggressive and accompanied by numerous microglia/macrophages (MG/MP) in and about the tumor. Little is known about what MG/MP do in this setting, or whether modulating MG/MP activation might affect glioma progression. Here, we used a glioma-microglia in culture system to establish the effects the tumor and microglia have on each other. We assessed glioma progression in vivo after MG/MP ablation or in the setting of exaggerated MG/MP activation. We show that glioma cells activate microglia but inhibit their phagocytic activities. Local ablation of MG/MP in vivo decreased tumor size and improved survival curves. Conversely, pharmacological activation of MG/MP increased glioma size through stimulating tumor proliferation and inhibiting apoptosis. In agreement with recent reports, expression of the chemokine CCL21 is enhanced after MG/MP activation and correlates with tumor growth. Taken together, our findings demonstrate that inhibition of MG/MP activation may constitute a new and effective contribution towards suppressing glioma proliferation.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

P157: Periostin Recruits Tumor Associated Macrophages in Glioblastoma Multiform

Glioblastoma multiform (GBM) is the most common and lethal type of primary brain tumors with high rates of morbidity and mortality. Treatment options are limited and ineffective in most of the cases. Epidemiological studies have shown a link between inflammation and glioma genesis.  In addition, at the molecular level, pro-inflammatory cytokines released from activated microglia can increa...

متن کامل

O27: Interaction of Cancer Stem Cells and Microglia in Glioblastoma Multiforme

Malignant gliomas are highly invasive brain tumors with the occurrence of multiple microglia/macrophages in the tumor microenvironment. Macrophages/microglia that found in glioma microenvironment, as tumor-infiltrating immune cells, can play a harmful role in tumor progression. In addition, glioblastoma multiforme (GBM) contains multiple aberrant differentiation and tumorigenic cancer stem cell...

متن کامل

Microglia-glioma cross-talk: a two way approach to new strategies against glioma.

Glioblastoma (GBM) is the most malignant and aggressive among primary brain tumors, characterized by very low life expectancy. In vivo, glioma and glioblastoma in particular contain large numbers of immune cells (myeloid cells) such as microglia and tumour-infiltrating macrophages (or glioma associated macrophages). These glioma-infiltrating myeloid cells comprise up to 30% of total tumor mass ...

متن کامل

F11R Is a Novel Monocyte Prognostic Biomarker for Malignant Glioma

OBJECTIVE Brain tumors (gliomas) contain large populations of infiltrating macrophages and recruited microglia, which in experimental murine glioma models promote tumor formation and progression. Among the barriers to understanding the contributions of these stromal elements to high-grade glioma (glioblastoma; GBM) biology is the relative paucity of tools to characterize infiltrating macrophage...

متن کامل

Microenvironment and Immunology RAGE Expression in Tumor-Associated Macrophages Promotes Angiogenesis in Glioma

Interaction of RAGE (the receptor for advanced glycation endproducts) with its ligands can promote tumor progression, invasion, and angiogenesis. Although blocking RAGE signaling has been proposed as a potential anticancer strategy, functional contributions of RAGEexpression in the tumormicroenvironment (TME) havenot been investigated in detail. Here, we evaluated the effect of genetic depletio...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Glia

دوره 59 3  شماره 

صفحات  -

تاریخ انتشار 2011