Project description:Exosomal miRNAs including 86 exosomal miRNAs were significantly increased and 354 exosomal miRNAs were significantly decreased in the co-injection group compared to LLC injection alone through expression profiling of a total of 1903 genes.
Project description:MiRNA microarray analysis was performed on exosomes secreted by mouse MSC cells under two different conditions of normal oxygen and hypoxia, in order to find out the different miRNAs in exosomes secreted by MSC under two different conditions.
Project description:PBS and Il-5 (22 pM) treated LLC and B16 cells were harvested after 24 hours, for comparison between: 1) PBS and IL-5 trerated LLC cells, and 2) btween LLC and B16 cells at baseline conditions.
Project description:To further development of our miRNA diagnostic approach to Kawasaki disease(KD), we have employed microRNA microarray expression profiling as a discovery platform to identify microRNAs as the potential biomarkers to rapidly diagnose Kawasaki disease. Pooled exosome of serum in equal amount from 5 healthy children, 5 KD patients and 5 KD patients after Intravenous immunoglobulin (IVIG) therapy were used for microRNA microarray analysis. MicroRNA profile of exosome from Kawasaki disease(KD) was analyzed by microRNA microarray analysis in 5 healthy children, 5 KD patients and 5 KD patients after IVIG therapy.
Project description:Background: We and others have previously demonstrated the potential for circulating exosome microRNAs to aid in disease diagnosis. In this study, we sought the possible utility of serum exosome microRNAs as biomarkers for disease activity in multiple sclerosis patients in response to fingolimod therapy. We studied patients with relapsing-remitting multiple sclerosis prior to and 6 months after treatment with fingolimod. Methods: Disease activity was determined using gadolinium-enhanced magnetic resonance imaging. Serum exosome microRNAs were profiled using next-generation sequencing. Data were analysed using univariate/multivariate modelling and machine learning to determine microRNA signatures with predictive utility. Results: we identified 15 individual miRNAs that were differentially expressed in serum exosomes from post-treatment patients with active versus quiescent disease. The targets of these microRNAs clustered in ontologies related to the immune and nervous systems, and signal transduction. While the power of individual microRNAs to predict disease status post-fingolimod was modest (average 77%, range 65 to 91%), several combinations of 2 or 3 miRNAs were able to distinguish active from quiescent disease with greater than 90% accuracy. Further stratification of patients identified additional microRNAs associated with stable remission, and a positive response to fingolimod in patients with active disease prior to treatment. Conclusions: Overall, these data underscore the value of serum exosome microRNA signatures as non-invasive biomarkers of disease in multiple sclerosis and suggest they may be used to predict response to fingolimod in future clinical practice. Additionally, these data suggest that fingolimod may have mechanisms of action beyond its known functions.