Background Extracellular matrix (ECM)-components serve as a storage site to
concentrate and stabilise growth factors in the vicinity of cells. Human u
mbilical cord (UC) tissues contain significant amounts of IGF-I and IGF-bin
ding proteins (BPs). IGF-I is known as a stimulator of collagen and sulphat
ed glycosaminoglycans (GAGs) biosynthesis. Pre-eclampsia, the most common p
regnancy associated syndrome, is accompanied by an accumulation of collagen
and sulphated glycosaminoglycans in the UC. One may expect that IGF-I and
BPs play an important role in such a remodelling of the UC tissue. For this
reason it was decided to evaluate the alterations in amounts of IGF-I and
BPs in UC serum and in the UC arterial wall of newborns delivered by mother
s with pre-eclampsia.
Materials and methods Studies were performed on the UCs of 12 control and 1
2 investigated newborns, delivered by mothers with pre-eclampsia (edema, pr
oteinuria > 500 mg l(-1), arterial pressure: systolic > 140 mmHg, diastolic
> 100 mmHg). Radioimmunological techniques were employed to determine IGF-
I and IGF-BPs (BP-1 and BP-3).
Results It was found that pre-eclampsia is associated with an increase of I
GF-I concentration in the UC serum and with simultaneous decrease of its co
ntent in the umbilical cord artery (UCA). The decrease of IGF-I content in
the UCA wall was accompanied by an increase of BP-3 and BP-1 in this tissue
. The increase in BPs content in the UCA wall was not associated with an en
hancement of IGF binding by extracts from the homogenates of arterial wall.
Heparin drastically decreased the binding of IGF-I by BP-3.
Conclusions Pre-eclampsia is associated with an increase of IGF-I-concentra
tion in the umbilical cord blood and an elevation of BPs contents in the UC
A wall. Despite a high concentration of binding proteins, IGF-I is not accu
mulated in this tissue. High amounts of sulphated GAGs in the UCA wall may
be a factor that prevents the binding of IGF-I by BPs. Free IGF-I can easil
y bind to cell receptors and stimulate the cells to produce collagen and su
lphated GAGs in the arterial wall.