Transcription profiling of human miRNA expression in mesenchymal stem cells in young and old donors.
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ABSTRACT: Mesenchymal stem cells were isolated from several donors of different age (young vs old), and total RNA was extracted. Samples were labeled with Cy3 and Cy5 dyes and hybridized in a looped design that allowed the calculation of differentially expressed miRNAs in MSCs isolated from healthy, aged individuals.
Project description:Foreskin samples were derived from young and old donors. Total RNA was extracted and used for hybridization to microRNA microarrays. From 4 young and 4 old donors, differential expression of microRNAs was analyzed using R/Bioconductor and linear models
Project description:From two donors of human umbilical vein endothelial cells, in vitro cell lines were established. Both cell lines were grown in vitro until irreversible growth arrest was observed (replicative senescence). Total RNA from young (replicating) cells as well as senescent cells was harvested and used for hybridization of microRNA chips (MRC) from TU Graz based on Sanger miRBase 9.2
Project description:T cells from several blood donors were separated in populations corresponding to CD8+ CD28+ and CD8+ CD28- surface markers. Total RNA extracts from cells were hybridized to MRC LNA microarray. Contrasts of interest were CD8CD28- minus CD8CD28+ (replicative aging) and CD8CD28+ (old donors) minus CD8CD28+ (young donors), which corresponds to chronological aging.
Project description: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:The transcriptome of two different Pseudomonas aeruginosa mutant strains were compared to the Pseudomonas aeruginosa wild type strain in the stationary growth phase
Project description:Cy3 and Cy5 direct labelled RNA from Bloodstream MiTat1.1 trypanosomes and Procyclic 427 Lister were hybridized onto JCVI Trypanosoma brucei oligoarrays (version2). Procyclic RNA were used as control for data analysis.
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:Experimental Description<br><br>Mice overexpressing lymphotoxin alpha and beta, mice overexpressing lymphotoxin alpha and beta with concomitant hepatocyte-specific knock-out of the IKK-beta gene, and wild type C57BL/6 mice were sacrificed at 3 and 9 months of age, resp. From the respective livers, mRNA was extracted and whole genome transcription profiling was conducted with hybridization on day 1,2 or 3.