Transcription profiling by array of human olfactory ecto-mesenchymal stem cells in familial dysautonomia
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ABSTRACT: Exploration of transcriptome expression in 5 control and 4 familial dysautonomia (FD) human olfactory ecto-mesenchymal stem cells (hOE-MSCs) at very early (P1 and P2) and later (P5 and P9) cell passages.
Project description:HBEC-5i (human brain endothelial cells) grown to confluence in 6-well tissue culture plates. Cocultures were either left unstimulated or incubated overnight with recombinant TNF?. HBEC were then washed in PBS and incubated with PLT (platelets), pRBC (P.falciparum-parasited red blood cells) or NRBC (normal red blood cells) according to the experimental conditions. Then HBEC were washed three times with PBS, and were harvested at 0 and 5h coculture. Each experimental condition was realized in triplicate.
Project description:To study the composition of mRNPs containing TcDhh1, we carried out immunoprecipitation assays with anti-TcDhh1 and epimastigotes lysates. Pre-immune serum was used as control. We also carried out a ribonomic approach to identify the mRNAs present within the TcDhh1 immunoprecipitated complexes. For this purpose, competitive microarray hibridizations were performed against negative controls, the non-precipitated fraction.
Project description:Four independent pools of zebrafish embryo were injected with prp2 morphants and after 24 hours post fertilization, gene expression profiles were compared to their respective controls, using microarray. A dye swap design experiment using four microarray slides were conducted.
Project description:<br><br>Annual heart allograft failure in humans rates about 3-5%. The main reason after the first postoperative year is chronic rejection. Myointimal hyperplasia, the hellmark of chronic rejection, results in a specific type of ischemic heart disease. The lack of angina pectoris symptoms allow ventricular arrythmias, sudden cardiac death or heart failure to occur without warning. In addition, diagnostic tools such as endomyocardial biopsy, coronary angiography or intracoronary ultrasound fail to predict the individual risk for myocardial dysfunction.<br><br>The mechanisms responsible for chronic rejection are predominantly alloimmune mediated with activated T cells, macrophages, B cell mediated antibody formation and secreted cytokines responding to HLA and other endothelial cell antigens. In addition, non immunologic risk factors such as recipient age, metabolic factors, hypertension and ischemia contribute to development of this disease. Previous studies have demonstrated that ischemia has a profound influence on short term allograft survival but the underlaying mechanisms remain largely unknown. Apoptosis seems to play a crucial role in ischemia/reperfusion injury and several mechanisms for programmed cell death have been described. However, consequences on long term cell function of viability have not been investigated. <br><br>The aim of this study was to investigate the implication and the mechanism of prolonged cold organ storage as a non immunologic risk factor in the pathogenesis of chronic rejection in a cardiac allograft model. <br><br>We aimed for answering the following specific questions:<br><br>How does cold ischemia affect the alloimmue response short and long term? <br><br>How does prolonged cold ischemia affect gene expression at later time points after transplantation? <br><br>Does it influence gene expression during chronic rejection?<br><br><br><br>
Project description:comparison of gene expression between UV-B irradiated Physcomitrella patens gametophores with their non-irradiated controls in two different UV irradiation fields.
Project description:Microarray analyses allow the identification and assessment of molecular signatures in whole tissues undergoing pathological processes. To better understand cerebral malaria pathogenesis, we investigated intra-cerebral gene-expression profiles in well-defined genetically cerebral malaria-resistant (CM-R) and CM-susceptible (CM-S) mice, upon infection by Plasmodium berghei ANKA. We investigated mouse transcriptional responses prior to infection, and at early and late stages of infection by use of cDNA microarrays. Through a rigorous statistical approach with multiple testing corrections, we showed that P. berghei ANKA significantly altered brain gene expression in CM-R (BALB/c), and in CM-S (CBA/J and C57BL/6) mice, and that 327 genes discriminated between early and late infection stages, between mouse strains, and between CM-R and CM-S mice. We further identified 104, 56, 84 genes with significant differential expression between CM-R and CM-S mice on days 2, 5, and 7 respectively. The analysis of their functional annotation suggests that genes involved in metabolic energy pathways, the inflammatory response, and the neuroprotection/neurotoxicity balance play a major role in cerebral malaria pathogenesis. In particular, we evidenced the down-regulation of genes involved in oxidative phosphorylation and the Reln pathway, and the up-regulation of genes involved in the NF-kB signalling pathway in CM-S mice. In addition, our data suggest that cerebral malaria and Alzheimers disease may share some common mechanisms of pathogenesis, as illustrated by the accumulation of beta-amyloid proteins in brains of CM-S mice, but not of CM-R mice. Our results indicate that microarray analyses can provide new insights into the key events that govern malaria pathogenesis.