%0 Journal Article
%T Matrix metalloproteinase-2 is elevated in midtrimester amniotic fluid prior to the development of preeclampsia
%A Michal Lavee
%A Shlomit Goldman
%A Etty Daniel-Spiegel
%A Eliezer Shalev
%J Reproductive Biology and Endocrinology
%D 2009
%I BioMed Central
%R 10.1186/1477-7827-7-85
%X Amniotic fluid was obtained from 133 women undergoing genetic second trimester amniocentesis. Zymography was performed for MMP characterization and an MMP-2 ELISA kit was used to determine MMP-2 levels. TIMP-2 expression was evaluated using western blot.Mean amniotic fluid MMP-2 and TIMP-2 levels were significantly higher in women who developed a hypertensive disorder compared to normotensive women (P < 0.0004 and P < 0.01, respectively). When subdivided into subgroups, amniotic fluid from women who eventually developed preeclampsia or superimposed preeclampsia showed significantly higher MMP-2 levels than normotensive women (P < 0.05). However, no statistical difference in MMP-2 levels was found between patients with gestational hypertension and normotensive patients.Higher amniotic fluid MMP-2 and TIMP-2 levels are found in women who eventually develop preeclampsia.Preeclampsia is a multi-system disorder of pregnancy characterized by hypertension, proteinuria and generalized systemic vasoconstriction. The disorder is diagnosed in the latter half of pregnancy, effects about 5% of pregnancies and accounts for considerable mortality and morbidity [1].Several models have been proposed for the pathogenesis of preeclampsia. [2-4]. Prevailing evidence suggest insufficient trophoblast invasion of the maternal spiral arteries as the main pathogenesis of the disease. Whereas in normal pregnancy the luminal diameter of the spiral arteries is greatly increased and the vascular smooth muscle is replaced by trophoblast cells, in preeclamptic pregnancies this process is deficient. The resulting under-perfused placenta attempts to compensate by promoting the secretion of factors into the maternal circulation causing systemic alterations in endothelial cell function, accounting for the clinical syndrome of preeclampsia. Although this hypothesis is widely accepted, the molecular mechanisms that regulate this pathological process are still controversial.The role of matrix metallopro
%U http://www.rbej.com/content/7/1/85