Glycosaminoglycan-biosynthesis in the wall of the umbilical cord artery and its alteration in EPH-gestosis

The mechanism of edema, proteinuria, hypertension (EPH)-gestosis-associated premature replacement of hyaluronic acid by sulphated glycosaminaoglycans (GAGs) in the umbilical cord arteries is not known. It may result from altered biosynthesis, a different degradation rate or a combination of both phe...

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Published in:European journal of obstetrics & gynecology and reproductive biology Vol. 72; no. 1; pp. 19 - 25
Main Authors: Romanowicz, Lech, Bańkowski, Edward, Galewska, Zofia, Jaworski, Stefan
Format: Journal Article
Language:English
Published: Shannon Elsevier Ireland Ltd 01-03-1997
Elsevier
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Summary:The mechanism of edema, proteinuria, hypertension (EPH)-gestosis-associated premature replacement of hyaluronic acid by sulphated glycosaminaoglycans (GAGs) in the umbilical cord arteries is not known. It may result from altered biosynthesis, a different degradation rate or a combination of both phenomena. In order to solve this problem, it was decided to evaluate the biosynthesis and degradation of newly synthesized GAGs in the umbilical cord arteries of control newborns and those delivered by mothers with EPH-gestosis. Incorporation of radioactive precursors ([ 14C]glucosamine and [ 35S]sulphate) into GAGs and degradation of newly synthesized GAGs using the pulse-chase experiment were evaluated. We found that the investigated tissue slices incorporated distinctly less [ 14C]glucosamine into hyaluronic acid in comparison to controls. In contrast to that, the biosynthesis of sulphated GAGs did not change significantly. However, the degradation of newly synthesized sulphated GAGs was distinctly slower than in control tissues. It may be concluded that an EPH-gestosis associated decrease in hyaluronic acid content in the umbilical cord artery is a result of decreased biosynthesis of this substance, whereas an increase in sulphated GAGs-content is rather a result of slower degradation of newly synthesized GAGs.
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ISSN:0301-2115
1872-7654
DOI:10.1016/S0301-2115(96)02651-6