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DOI 10.1159/000055936

Медицинская библиотека · Pathobiology : journal of immunopathology, molecular and cellular biology · 2000

Stimulation of glycosaminoglycan biosynthesis by umbilical cord serum of newborns delivered by mothers with EPH gestosis (preeclampsia).

Romanowicz L, Bańkowski E, Jaworski S

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVE

Edema, proteinuria, hypertension (EPH) gestosis, also known as preeclampsia, is the most common, pregnancy-associated pathological syndrome. It is accompanied by a significant increase in collagen content in the umbilical cord arteries and early replacement of hyaluronic acid by sulfated glycosaminoglycans (GAGs) both in these arteries and in Wharton's jelly. Such a remodelling of the umbilical cord tissues is accompanied by an increase in insulin-like growth factor-I (IGF-I) concentration in the umbilical cord serum.

METHODS

Contact-inhibited human fibroblasts were incubated in Dulbecco culture medium containing control or EPH umbilical cord serum and supplemented with (14)C-glucosamine or (35)S-sulfate. Radioactive GAGs were isolated, submitted to electrophoretic fractionation and quantified.

RESULTS

The presence of umbilical cord serum in culture medium strongly stimulated the incorporation of (14)C-glucosamine and (35)S-sulfate into GAGs synthesized by these cells. EPH serum was much more active in stimulation of sulfated GAGs biosynthesis than control serum, whereas the biosynthesis of hyaluronic acid was stimulated by both sera to a similar degree.

CONCLUSION

Since IGF-I is known as a stimulator of collagen and sulfated GAG biosynthesis, the high concentration of this growth factor in the umbilical cord plasma may be responsible for preeclampsia-associated remodeling of the umbilical cord.

Для цитирования: Romanowicz L, Bańkowski E, Jaworski S. Stimulation of glycosaminoglycan biosynthesis by umbilical cord serum of newborns delivered by mothers with EPH gestosis (preeclampsia).. Pathobiology : journal of immunopathology, molecular and cellular biology. 2000. DOI: 10.1159/000055936.

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