Project description:Background; Mutations in STOX1 were proposed as causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies. However, after the first study published in 2005 three other groups have dismissed the polymorphism described in the first paper as a causal mutation. Methodology and Principal Findings; In the present study, we have developed a choriocarcinoma cell line overexpressing STOX1. This overexpression results in the transcriptional modification of 12.5% of the genes, some of them being direct targets as shown by chromatin immunoprecipitation. STOX1 overexpression correlates strongly and specifically with transcriptomic alterations in preeclamptic placentas (r=0.30, p=9.10-7). Numerous known key modulators of preeclampsia (such as Endoglin, Syncytin, human chrionic gonadotrophin-hCG-, and Glial Cell Missing Homolog -GCM1-) were modified in these transformed choriocarcinoma cells. Conclusions; Our results contribute to reconcile contradictory data about the involvement of STOX1 in preeclampsia. In addition, they strongly suggest that anomalies in STOX1 expression are associated with the onset of preeclampsia, thus indicating that this gene should be the target of future studies. Furthermore, our cellular model could constitute an invaluable resource for studying specific aspects of this human disease. Experiment Overall Design: Microarrays expression
Project description:Background Mutations in STOX1 were proposed as causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies. However, after the first study published in 2005 three other groups have dismissed the polymorphism described in the first paper as a causal mutation. Methodology and Principal Findings In the present study, we have developed a choriocarcinoma cell line overexpressing STOX1. This overexpression results in the transcriptional modification of 12.5% of the genes, some of them being direct targets as shown by chromatin immunoprecipitation. STOX1 overexpression correlates strongly and specifically with transcriptomic alterations in preeclamptic placentas (r=0.30, p=9.10-7). Numerous known key modulators of preeclampsia (such as Endoglin, Syncytin, human chrionic gonadotrophin-hCG-, and Glial Cell Missing Homolog -GCM1-) were modified in these transformed choriocarcinoma cells. Conclusions Our results contribute to reconcile contradictory data about the involvement of STOX1 in preeclampsia. In addition, they strongly suggest that anomalies in STOX1 expression are associated with the onset of preeclampsia, thus indicating that this gene should be the target of future studies. Furthermore, our cellular model could constitute an invaluable resource for studying specific aspects of this human disease.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:The purpose of this study was to perform a comprehensive analysis of gene expression profile in placentas from preeclamptic pregnancies vs normal placentas.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
