Metabolism of glycosylated human salivary amylase: In vivo plasma clearance by rat hepatic endothelial cells and in vitro receptor mediated pinocytosis by rat macrophages

T. E. Niesen, D. H. Alpers, P. D. Stahl, J. L. Rosenblum

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17 Scopus citations

Abstract

Salivary-type amylase normally comprises about 60% of the amylase activity in human serum, but only a small fraction is a glycosylated isoenzyme (amylase A). In contrast, 1/3 of amylase in human saliva is glycosylated. Since glycosylation can affect circulatory clearance, we studied the clearance of amylase A in rats and its uptake by rat alveolar macrophages. Following intravenous injection, 125I-labeled amylase A disappeared rapidly from plasma (t 1/2 = 9 min) and accumulated in the liver. Simultaneous injection of mannose-albumin slowed its clearance to a rate comparable to that of 125I-labeled nonglycosylated salivary amylase (t 1/2 = 45 min). In contrast, galactose-albumin had no effect. Electron microscope autoradiography of the liver following injection of 125I-labeled amylase A revealed a localization of grains over the hepatic endothelial cells. In vitro studies indicated that amylase A is taken up by alveolar macrophages via receptor-mediating pinocytosis. Uptake was linear over time, saturable, and inhibited by mannan and mannose-albumin, but not by galactose-albumin. We conclude that amylase A, which is a naturally occurring human glycoprotein with at most three terminal L-fucose residues per molecule, is recognized in rats by a mannose receptor located on hepatic endothelial cells. We speculate that this receptor, by rapidly clearing circulating amylase A, may be responsible for the low level of amylase A in human serum.

Original languageEnglish
Pages (from-to)307-320
Number of pages14
JournalJournal of Leukocyte Biology
Volume36
Issue number3
DOIs
StatePublished - 1984

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