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- W2017272890 abstract "• oxLDL induces MMP-9 expression in mouse microglia. • oxLDL upregulates MMP-9 expression via TLR2 signaling pathway. • TLR2-dependent NO synthesis is required for MMP-9 expression. • TLR2 and NO mediate the stimulus-activated microglial neurotoxicity. Microglia are neural immune cells that produce pro-inflammatory proteins in the central nervous system. Dysregulation of microglia gene expression is linked to the chronic brain inflammation and the neurological disorders. Matrix metalloproteinase-9 (MMP-9) is a pro-inflammatory protease that regulates the neurotoxicity of glial cells in the brain and spinal cord. Recent studies showed the accumulation of MMP-9 at microglia-rich plaques associates with neurodegenerative diseases. However, the regulatory mechanism of MMP-9 expression in microglia inflammation is still unknown. Here we show that oxidized low-density lipoprotein (oxLDL) induces the expression and secretion of Pro-MMP-9 (92 kDa) via TLR2 signaling pathway in mouse microglial cells. Depletion of TLR2 or its signaling mediators MyD88/TRAF6 blocks the agonist-induced MMP-9 expression. In addition, TLR2-dependent nitric oxide (NO) synthesis is also required for endogenous Pro-MMP-9 expression and secretion. Cell death assay indicates that the neurotoxicity of microglia is regulated by endogenous NO and TLR2 signaling pathway. Our findings establish a pathophysiological link between oxLDL and MMP-9 expression in microglia-related neuroinflammation." @default.
- W2017272890 created "2016-06-24" @default.
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- W2017272890 date "2014-06-01" @default.
- W2017272890 modified "2023-09-27" @default.
- W2017272890 title "TLR2 signaling directs NO-dependent MMP-9 induction in mouse microglia" @default.
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- W2017272890 doi "https://doi.org/10.1016/j.neulet.2014.04.025" @default.
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