Project description:We report that miRNA-146a exerts anti-proliferative effects on endothelial cells in vitro as well as in vivo. In order to obtain insights into potential target genes, we generated samples of HUVEC overexpressing miRNA-146a and RNA sequencing was performed by Novogene (Novogene Bioinformatics Technology, Beijing, China)
Project description:We report that miRNA-146a exerts anti-proliferative effects on smooth muscle cells in vitro as well as in vivo. In order to obtain insights into potential target genes, we generated samples of SMC overexpressing miRNA-146a and RNA sequencing was performed by Novogene (Novogene Bioinformatics Technology, Beijing, China)
Project description:Human vein umbilical endothelial cells (HUVEC) were transfected with pre-miR control and pre-miR 146 (Ambion) in order to identify targets (direct and indirect) downregulated by miR-146a in endothelial cells. 164 transcripts were downregulated with a fold change ≥ 1.2. Total RNA was obtained from cells transfected in HUVEC with pre-miR control and pre-miR 146a. Three independent transfections were performed for each condition. 2 replicates for control re-control and 3 for pre-miR 146a were analyzed.
Project description:screenning the differentially expressed genes of Jurkat-FF3, Jurkat-miR146a, Jurkat-miR146a-sponge cell lines. To investigate the role of miR-146a on Jurkat T cells, we screened the differentially expressed genes of Jurkat-FF3 (as control), Jurkat-miR146a (as miR-146a overexpression cell line), Jurkat-miR146a-sponge (as miR-146a knock down cell line).
Project description:This study was designed to explore the role of miRNA-146a (miR-146a) and its target genes in the endothelial cells. In this study we have demonstrated that lipopolysaccharide (LPS) induced upregulation of miR-146a in the human umbilical vein endothelial cells (HUVEC) and the induction was blocked by the silencing of the toll-like receptors (TLRs) adaptor molecules MyD88 and nonspecific NF-κB inhibitor BAY 11-7082. In addition, knockdown of miR-146a by transfection of the locked nucleic acid (LNA)-antimiR-146a significantly decreased the increased cell migration and tube formation induced by LPS. A combined analysis of the bioinformatics miRanda algorithms and the whole genome expression microarray of the immunoprecipitated Ago2 ribonucleoprotein complex identified 14 transcripts as the potential target genes. Subsequent transfection with miR-146a precursor pre-miR-146a into the HUVEC validated that the CARD10 was the target gene of the miR-146a both in the transcript and protein level.
Project description:MiR-146a is an important regulator of innate inflammatory responses and is also implicated in cell death and survival. Here, we identified microglia as the main cellular source of miR-146a among mouse CNS resident cells. We further characterized the phenotype of miR-146a KO microglia cells during in vivo demyelination induced by cuprizone (CPZ) and found reduced number of CD11c+ microglia in the KO compared to WT mice. Microglia were also isolated from the brain, and the proteome was analyzed by liquid chromatography mass spectrometry.
Project description:Human vein umbilical endothelial cells (HUVEC) were transfected with pre-miR control and pre-miR 146 (Ambion) in order to identify targets (direct and indirect) downregulated by miR-146a in endothelial cells. 164 transcripts were downregulated with a fold change ≥ 1.2.