Session Speaker

Angiogenic Factors and their Role in Uteroplacental Dysfunction
Loganath Annamalai, Roopa Kothapalli, Anupriya Gopalsamy, Kwee Lim Peh , Yee Chee Wong, Yap Seng Chong
Singapore

Hemochorial placental development involves invasion of the extravillous trophoblast cells into the uterine wall and subsequent remodeling of the uteroplacental vessels. Angiogenesis, the formation of new blood vessels from pre-existing endothelium, is a complex process necessitating the interactions of numerous cell types that lead to the coordinated development of a complex three-dimensional vascular structure in human placenta. Profound angiogenesis in the placenta is essential as high capacity transport is established between the maternal and fetal circulation. Among the most intensively studied angiogenic factors is the vascular endothelial growth factor family (VEGF) and placental growth factor (PlGF). Studies of circulating concentrations of VEGF in preeclampsia have reported conflicting results. However, it appears that only free VEGF is biologically active and available to interact with cell surface receptors and possess relevant angiogenic activity.

Soluble Flt-1 (sFlt-1) has been shown to be increased in the placenta and blood of women with preeclampsia. In the continuing search for fundamental insights into placental angiogenesis, we have for the first time identified the mRNA expression and secretion of angiogenin, a single chain 14-kDa non-glycosylated polypeptide in normal placenta in a gestational dependent manner. Further investigations revealed overexpression of this angiogenic peptide in placentae of patients presenting with preeclampsia and fetal growth retardation.

The role of these vasculogenic factors remains unknown at present but could be attributed to the ability to circumvent the poor oxygenation resulting from defective fetoplacental blood flow by autoregulation and could serve as positive feedback regulators to induce neovascularization in these compromised pregnancies.