Varshavsky JR, Robinson JF, Zhou Y, Puckett KA, Kwan E, Buarpung S, Aburajab R, Gaw SL, Sen S, Gao S, Smith SC, Park JS, Zakharevich I, Gerona RR, Fisher SJ, Woodruff TJ.The Placenta - Fast, Loose, and in Control. Global proteomic analyses of human cytotrophoblast differentiation/invasion. Chen H, Williams KE, Kwan EY, Kapidzic M, Puckett KA, Aburajab RK, Robinson JF, Fisher SJ.RNA profiling of laser microdissected human trophoblast subtypes at mid-gestation reveals a role for cannabinoid signaling in invasion. Gormley M, Oliverio O, Kapidzic M, Ona K, Hall S, Fisher SJ.Establishment of fetomaternal tolerance through glycan-mediated B cell suppression. Rizzuto G, Brooks JF, Tuomivaara ST, McIntyre TI, Ma S, Rideaux D, Zikherman J, Fisher SJ, Erlebacher A.Bisphenol A replacement chemicals, BPF and BPS, induce protumorigenic changes in human mammary gland organoid morphology and proteome. Winkler J, Liu P, Phong K, Hinrichs JH, Ataii N, Williams K, Hadler-Olsen E, Samson S, Gartner ZJ, Fisher S, Werb Z.Regionally distinct trophoblast regulate barrier function and invasion in the human placenta. Marsh B, Zhou Y, Kapidzic M, Fisher S, Blelloch R. Vedolizumab Antagonizes MAdCAM-1-Dependent Human Placental Cytotrophoblast Adhesion and Invasion In Vitro. Blaisdell A, Zhou Y, Kattah MG, Fisher SJ, Mahadevan U.The goal of the third and newest project is to formulate novel methods that enable robust mass spectrometry-based platforms for the discovery of biomarkers in body fluid for the early detection of tumors. The second is an analysis of the primary proteome and protein complexes of the soil organism Desulfovibrio vulgaris. The first is compilation of an initial draft of the salivary proteome of healthy individuals as a first step in using this body fluid for diagnosis of common diseases. Our recently funded CIRM comprehensive grant is focused on constructing a fate map of the human embryo.įinally, we are using mass spectrometry-based approaches for proteome analyses. Currently we are investigating how this highly specialized phenomenon is related to pluripotency. We recently made the surprising discovery that the cells exhibit apical-basal type polarization. Our work to date has focused on deriving additional lines using feeders formed from human placental cells. In parallel, our lab has begun studying the earliest stages of human development using human embryonic stem cells as a model system. For example, our work shows that this pregnancy complication is characterized by specific aberrations in trophoblast secretion of vasculogenic/angiogenic substances. Finally, we use information about molecular aspects of cytotrophoblast function in normal pregnancy to search for defects that are associated with pregnancy complications such as preeclampsia (e.g., dangerously high blood pressure). Recently, we showed that oxygen controls whether cells proliferate or exit the cell cycle and differentiate Eph/ephrin family members, transmembrane ligands and receptors, pattern invasion in terms of arterial bias. What controls this highly unusual differentiation process? Since cytotrophoblasts target large-bore arterioles for invasion, we reasoned that oxygen tension could play a role. This phenomenon is likely to be a critical component of normal placentation. Additionally, we found that cytotrophoblasts that replace the endothelial lining of uterine blood vessels also have the amazing ability to mimic the adhesion phenotype of vascular cells. Function-perturbation experiments suggest that cytotrophoblasts carefully regulate their invasive potential by simultaneously expressing a number of molecules that either promote or inhibit invasion. Our studies show that, in normal pregnancy, cytotrophoblast invasion, both in vivo and in vitro, is accompanied by a dramatic switch in the cells' expression of matrix-degrading metalloproteinases and adhesion molecules. The cytotrophoblasts that form the fetal portion of the human placenta have solved this problem by transiently exhibiting certain invasive, tumor-like properties. Human fetal development depends on the embryo's ability to rapidly gain access to the maternal circulation. In the first, we are studying the mechanisms used by the trophoblast cells of the human placenta to invade the uterus during normal pregnancy.
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