reatment with nondecidualized CM. Certainly, treatment with non-decidualized CM upregulated DPP1 in EVT cell lysates; we were unable to detect DPP1 in EVT CM by western blotting and thus were unable to confirm the regulation of cell surface DPP1 by non-decidualized CM. Overall, our data suggests that the protease activity of DPP1 may be enhanced by non-decidualized CM. LAMP1, also known as CD107a, was recently identified in EVT where its expression correlated with the ability of EVT to resist infection from Listeria monocytogenes, suggesting that EVT may have a bactericidal phenotype. Certainly, NK cells which express LAMP1 are `degranulating’, ie. they are secreting antimicrobial cytotoxic molecules. Our co-localization data showed HLAG negative, LAMP1 positive cells in the decidua, particularly surrounding un-remodelled blood vessels and the glandular epithelium. These cells did not co-localize with CD45 or CK7, suggesting that these cells are not leukocytes or HLAG negative trophoblast cells. It is interesting to speculate that these cells may be decidual cells involved in the removal of smooth muscle from around spiral arteries. Here, using a novel in vitro and proteomics approach we have identified a number of proteins which were previously unknown to be expressed by EVT. This approach also identified a number proteins previously associated with diseases of pregnancy, in particular preeclampsia, suggesting that this approach can identify proteins which may have diagnostic or therapeutic potential for targeting these diseases. Previous studies have Odanacatib chemical information demonstrated that proteins which are produced at the fetal-maternal interface and regulate trophoblast invasion can be detected and in fact are dysregulated in maternal serum prior PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/22188860 to disease onset. Profilin 1, annexin A2 and DPP1 were identified for the first time in EVT and immunolocalized to interstitial EVT in 1st trimester decidua and placental villous. Further, the expression of profilin 1, annexin A2 and proDPP1 was regulated by HESC CM, indicating that the degree of decidualization may be important for EVT protein production. Interestingly, the two proteins identified as being up-regulated by non-decidualized CM are both associated with the activation of serine proteases and both induce a pro-inflammatory response, indicating that impaired decidualization may cause excess inflammation during iEVT invasion. Overall, we have demonstrated that our unique culture method coupled with a proteomics approach has significant potential to Decidual Factors Alter Trophoblast Proteins identify novel proteins expressed by EVT and to uncover the mechanisms leading to disease states. Acknowledgments The authors would like to thank Sister Judi Hocking and Virginia Lay for their excellent assistance. EMM received travel support from The CASS Foundation. PHI Data Audit 1123. Supporting Information ~~ Prostatic adenocarcinoma is a 
leading cause of death among men in the United States and Western Europe. Because of its androgen-dependent growth, hormone ablation remains the main treatment of metastatic disease. While initially effective, this treatment is followed in a few years by tumor recurrence in which an androgen-independent neuroendocrine subpopulation of cells is thought to play an important role. NE cells are quiescent, terminally differentiated cells characterized by dendrite-like processes extending between adjacent cells and by the expression of neuronal-like proteins such as CD56 and chro
