Our previous studies have demonstrated that preeclampsia causes a decrease in MMP-1, MMP-3, MMP-2 and MMP-9 content from the umbilical cord artery (UCA). These enzymes and their inhibitors (TIMPs) participate in remodelling of UCA extracellular matrix. They may by involved in the preeclampsia-associated increase in the collagen content in the UCA wall and other fetal arterial vessels. MMP-2, MMP-9 and their inhibitors (TIMP-1 and TIMP-2) play an important role in vascular remodelling and are implicated in pathological fibrosis. Alterations in those enzymes activity may contribute to the pathophysiology of preeclampsia. We have hypothesised that these enzymes and their inhibitors could be present in umbilical cord blood, and that the concentration of these proteins could have effects on both vascular remodelling and vascular reactivity. The effect of preeclampsia on the content and activity of metalloproteinases in umbilical cord blood serum and plasma was elevated by immunoenzymatic methods and zymographic technique. A high amount of MMP-2 (gelatinase A), MMP-9 (gelatinase B), TIMP-1 and TIMP-2 was detected in all investigated fluids. Preeclampsia is associated with a distinct increase in MMP-9 content in umbilical cord blood plasma. The amount of TIMPs is so high enough to inhibit the activity of MMPs. It can be concluded from zymography that MMP-2 (gelatinase A) is present as proenzymatic form in both control and preeclamptic umbilical cord blood. Control umbilical cord plasma does not demonstrate activity of MMP-9 only, even after activation with APMA. High content of investigated metalloproteinases and their inhibitors in the umbilical cord blood may be a result of releasing those proteins from vessel wall cells. It can be concluded that an increase in MMP-9 concentration in umbilical blood, in turn, can alter vascular function in newborns delivered by mothers with preeclampsia.

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1. Sphingomyelins and ceramides of umbilical cord tissues and their alterations in preeclampsia