Searchable abstracts of presentations at key conferences in endocrinology

ea0019p109 | Cytokines and growth factors | SFEBES2009

Quantum dot labelled IGF-I: a novel technique to study IGF-signal transduction in the human placenta

Forbes K , Aplin J , Westwood M

In humans, the exchange of nutrients and waste between mother and fetus occurs via the outer layer of the placenta (syncytium; ST); this layer is maintained by continuous growth and differentiation of underlying cytotrophoblasts (CT). Pregnancy complications such as intrauterine growth restriction are associated with abnormal CT proliferation and apoptosis; altered levels of maternal insulin-like growth factors (IGFs) have also been reported in these conditions. We have demons...

ea0003oc21 | Growth Regulation | BES2002

Decidual matrix metalloproteases MMP-3 and MMP-9 proteolyse insulin-like growth factor binding protein-1

Coppock H , Aplin J , White A , Westwood M

Growth in utero depends on adequate development and function of the fetal / maternal interface. During pregnancy, the insulin-like growth factors (IGFs), which are known to be critically involved in placental development, are controlled by a binding protein - IGFBP-1 - produced by maternal decidualised endometrium. We have recently found that decidua also produces a protease which cleaves IGFBP-1 into fragments that are unable to bind ligand. This study aimed to identif...

ea0019p288 | Reproduction | SFEBES2009

IGF-2 receptor signalling and trophoblast cell turnover

Harris L , Aplin J , Baker P , Crocker I , Westwood M

Objective: Insulin-like growth factor-II (IGF-II), a critical regulator of placental development, enhances proliferation and survival of human cytotrophoblasts by signalling through the IGF-1 receptor (IGF-1R). Excess IGF-II binds to IGF-2R, which mediates its transport to the lysosomes for degradation. Although considered to act solely as an IGF-II clearance receptor, IGF-2R has been implicated in mediating IGF-II-stimulated migration and invasion in trophoblast. We therefore...