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Serum amyloid A (SAA) proteins were originally identified as prominent acute-phase serum proteins synthesized predominantly by hepatocytes. These small proteins are remarkably lipophilic, and we have sought evidence for their synthesis in mouse brain. RT-PCR showed constitutive expression of the murine SAA1 gene in the brains of normal BALB/cJ mice. After intracerebral inoculation with Sindbis virus, these mice predictably increase brain expression of tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), and IL-6. However, brain SAA1 expression fell after injecting either virus or control saline and remained low despite increases in TNF-alpha and IL-6, which are known to induce its expression in hepatocytes. Our data thus show that expression of the murine SAA1 gene has different, unprecedented control in mouse brain, suggesting that the protein itself may have a different physiological role there.
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Tucker et al. (2001) studied this question.
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