This seminar discusses a known complication of pregnancy called pre-eclampsia. The cause of this disorder is not completely understood but one of its key feature is the inadequate invasion of cells of the placenta called trophoblasts. Furthermore, current biomarkers of this disorder are poor and there is no none cure except delivery of the baby and the placenta. Glycosaminoglycans (GAGs) are co-receptors of some pro-survival growth factors and may be implicated in this disorder. In the study presented, GAGs are characterised in the placenta. Their biomarker potential and possible involvement in the pathogenesis of pre-eclampsia are assessed.
Preeclampsia is a multi-systemic and multifactorial disorder associated with 2-8% of pregnancies. Clinical presentation include significant proteinuria and arterial hypertension. These presentations are usually seen after the 20th week of gestation in previously normotensive women and the only known cure is delivery of the baby and the placenta. The proliferation and invasion of placental trophoblasts is vital to the success of pregnancies. Inadequate trophoblastic invasion is generally accepted as a key feature of pre-eclampsia. Glycosaminoglycans (GAGs) are anionic linear polysaccharides comprising major repeating disaccharide units of a uronic acid and an amino sugar. They play a vital role in anticoagulation, tumour growth and metastasis, cell signalling and angiogenesis. They serve as co-receptors for various placental growth factors hence their importance in trophoblast proliferation and invasion. The growth factor-binding ability of GAGs is influenced by numerous structural modifications of the GAG chain including sulphation. In the study presented here, GAGs were characterised in pre-eclampsia and their potential as biomarkers was investigated. The effect of various exogenous GAGs of defined length and sequence on trophoblast differentiation, invasion and proliferation was also investigated.
For more information, contact Senior Lecturer in Life Sciences Dr Britta Stordal
