Project description:To determine the possible role of SA in root meristem activity, we compared the gene expression profiles of the root tip of Osaim1 and WT under control condition and SA treatment. We used microarrays to detail the global programme of gene expression underlying control condition and SA treatment between WT and Osaim1 mutant.
Project description:MEcPP overaccumulation in the ceh1 mutant results in significant transcriptome changes as reported by microarrays, of which some are dependent on the SA accumulation in this mutant. In order to gain better resolution of transcriptomic changes in ceh1 as well as the SA dependence of these changes, we performed RNAseq analysis of RNA extracted from wt, ceh1, eds16 deficient in SA production, and ceh1/eds16
Project description:Microvascular endothelial cells play important roles in sepsis-associated acute kidney injury (SA-AKI). In this study, we focused on microvascular microRNAs changes following SA-AKI to identify microRNAs as novel druggable targets and microvasculature-related early biomarkers of SA-AKI. Using small RNA sequencing we identified 40 differentially expressed microRNAs in the renal microvasculature in response to SA-AKI. While the induction of most microRNAs was restricted to a single microvascular compartment, miR-21-5p levels were increased across the renal microvasculature in both mice and humans following SA-AKI. Functional assessment in vitro revealed that inhibition of hsa-miR-21-5p exacerbated endothelial inflammatory activation, suggesting a protective role of this microRNA in endothelial cells. Furthermore, patients with SA-AKI exhibited elevated hsa-miR-21-5p levels in plasma compared with critically ill sepsis patients without AKI. These results highlight the potential of hsa-miR-21-5p and other microRNAs as therapeutic targets and biomarkers in SA-AKI.
Project description:This model was reconstructed from single-nucleus RNA-seq (snRNA-seq) data of human postmortem brain and curated using published metabolomics data from human iPSC-derived neurons and cerebrospinal fluid (CSF), together with gene expression data from the Human Protein Atlas. It more accurately simulates human neuronal metabolic flux in neurodegenerative conditions such as Alzheimer's disease (AD).