Nov 15, 1989

Differential induction of the serum amyloid A gene family in response to an inflammatory agent and to amyloid-enhancing factor

The Journal of Biological Chemistry
L BrissetteR Deeley

Abstract

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.

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Mentioned in this Paper

Silver Nitrate, Silver (2+) Salt (2: 1)
Amyloid enhancing factor
APP protein, human
SAA2 gene
Spleen
Murine
Genes, Reiterated
Transcription, Genetic
Tissue Specificity
Argentum nitricum, silver nitrate

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