AI Article Synopsis
- The study investigates how glioma cells secrete factors that affect the activation of microglia, which are important immune cells in the brain.
- Conditioned medium from glioma cells significantly increases nitric oxide production and promotes the expression of various pro-inflammatory markers in microglial cells.
- The effects are mediated by the p38 MAPK pathway and nuclear factor-kappaB (NF-κB) signaling, suggesting that diffusible factors from gliomas play a role in shaping the tumor microenvironment and modulating immune responses.
Article Abstract
We aimed to elucidate the effect of soluble factors secreted by glioma on microglial activation. Conditioned medium (CM) from glioma cells, CRT-MG and C6, significantly induced nitric oxide (NO) production and stimulated the mRNA expression of inducible NO synthase (iNOS), interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF-α) and cyclooxygenase 2 (COX-2) in BV2 cells. Glioma CM stimulated p38 mitogen-activated protein kinase (MAPK) phosphorylation, and a p38 MAPK inhibitor, SB203580, suppressed CM-induced NO production in BV2 cells. In addition, CM stimulated nuclear factor-kappaB (NF-κB) DNA binding and transcriptional activity, which was repressed by SB203580. Gliomas displayed higher mRNA expression and release of TNF-α and IL-1β than primary astrocyte cells. Neutralization of TNF-α and IL-1β in C6-CM using a neutralizing antibody inhibited NO/iNOS expression in BV-2 cells. These results indicate potential contribution of diffusible tumor-derived factors to regulate microglial activation and subsequent tumor microenvironment.
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| http://dx.doi.org/10.1016/j.jneuroim.2016.08.001 | DOI Listing |
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