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• W2170147408 endingPage "97" @default.
• W2170147408 startingPage "89" @default.
• W2170147408 abstract "The pathological activation of microglia has been implicated in ischemic neuronal damage and some neurodegenerative diseases; however, the mechanism of microglial activation is not well understood. Previously, we showed that a serum factor, albumin, increased O(2)(-) production by cultured microglia (Si et al., 1997, Glia 21: 413-418). In the present study, we found that serum also enhanced lipopolysaccharide (LPS)-induced production of nitric oxide and tumor necrosis factor-alpha, which are other important neurotoxins released by activated microglia. In the presence of 0.1% normal rat serum, the half-effective concentration for LPS decreased from 300 to 1 ng/ml. The factor seemed to be a relatively high-molecular-weight protein because the factor was retained after a molecular sieve (50 kDa) membrane separation. The factor was labile to trypsinization and heat treatment at 72 degrees C for 5 min but was stable at 56 degrees C for 60 min. Several purified serum proteins including albumin could not mimic the enhancing effect of serum. Acute-phase serum showed a potent enhancing effect at a 10 times lower concentration than the normal serum. By gel filtration chromatography, the enhancing effect observed was a single peak at about 60 kDa. These results suggest that some serum protein infiltrates into brain parenchyma after blood-brain barrier disruption and such protein may result in neuronal damage by activating microglia to release neurotoxins in some central nervous system diseases." @default.
• W2170147408 created "2016-06-24" @default.
• W2170147408 creator A5029731768 @default.
• W2170147408 creator A5064164383 @default.
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• W2170147408 date "2000-03-01" @default.
• W2170147408 modified "2023-10-18" @default.
• W2170147408 title "A Serum Factor Enhances Production of Nitric Oxide and Tumor Necrosis Factor-α From Cultured Microglia" @default.
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• W2170147408 doi "https://doi.org/10.1006/exnr.2000.7334" @default.
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