Brissette L, Young I, Narindrasorasak S, Kisilevsky R, Deeley R
Cancer Research Laboratories, Queen's University, Kingston, Ontario, Canada.
J Biol Chem. 1989 Nov 15;264(32):19327-32.
The murine serum amyloid A1 (SAA1), SAA2, and SAA3 genes are expressed in various tissues in response to acute inflammation. Prolonged expression may be accompanied by amyloid deposition in liver, spleen, and kidney. Shortly before and during deposition, an amyloid-enhancing factor (AEF) can be extracted from these tissues which accelerates amyloid formation when administered with an inflammatory agent. We have investigated the ability of liver AEF to alter expression of the three SAA genes in liver, spleen, and kidney when administered to normal mice or to mice in which inflammation was created with the injection of silver nitrate. In liver, both AEF and silver nitrate induce SAA1 and SAA2 mRNA accumulation. However, AEF elicits a more rapid response and also acts as a potent inducer of hepatic SAA3 mRNA. Silver nitrate does not induce any SAA mRNA species in kidney, whereas AEF induces all three species. In contrast, AEF induces only SAA3 mRNA in the spleen. We also show that the elevation in hepatic SAA mRNA levels induced by either AEF or silver nitrate is associated with a transient increase in the length of the poly(A) tail.
小鼠血清淀粉样蛋白A1（SAA1）、SAA2和SAA3基因在急性炎症反应时会在多种组织中表达。长期表达可能会伴随肝脏、脾脏和肾脏中淀粉样蛋白沉积。在沉积前不久及沉积过程中，可从这些组织中提取出一种淀粉样蛋白增强因子（AEF），当与炎症因子一起给药时，它会加速淀粉样蛋白的形成。我们研究了将肝脏AEF给予正常小鼠或注射硝酸银引发炎症的小鼠后，其改变肝脏、脾脏和肾脏中三种SAA基因表达的能力。在肝脏中，AEF和硝酸银均能诱导SAA1和SAA2 mRNA积累。然而，AEF引发的反应更快，并且还是肝脏SAA3 mRNA的强效诱导剂。硝酸银在肾脏中不诱导任何SAA mRNA种类，而AEF能诱导所有三种。相反，AEF在脾脏中仅诱导SAA3 mRNA。我们还表明，AEF或硝酸银诱导的肝脏SAA mRNA水平升高与多聚腺苷酸（poly(A)）尾长度的短暂增加有关。
