Why are some amyloidoses systemic? Does hepatic "chaperoning at a distance" prevent cardiac deposition in a transgenic model of human senile systemic (transthyretin) amyloidosis?

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
Joel N BuxbaumDaniel R Salomon

Abstract

In the human systemic amyloidoses caused by mutant or wild-type transthyretin (TTR), deposition occurs at a distance from the site of synthesis. The TTR synthesized and secreted by the hepatocyte circulates in plasma, then deposits in target tissues far from the producing cell, a pattern reproduced in mice transgenic for multiple copies of the human wild-type TTR gene. By 2 yr of age, half of the transgenic males show cardiac deposition resembling human senile systemic amyloidosis. However, as early as 3 mo of age, when there are no deposits, cardiac gene transcription differs from that of nontransgenic littermates, primarily in the expression of a large number of genes associated with inflammation and the immune response. At 24 mo, the hearts with histologically proven TTR deposits show expression of stress response genes, exuberant mitochondrial gene transcription, and increased expression of genes associated with apoptosis, relative to the hearts without TTR deposition. These 24-mo-old hearts with TTR deposits also show a decrease in transcription of inflammatory genes relative to that in the younger transgenic mice. After 2 yr of expressing large amounts of human TTR, the livers of the transgenic mice without cardiac deposi...Continue Reading

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