Project description:We report the transcriptomic information of wild type (Lab-WT) A.baumannii 98-37-09 and A1S_3277 transposon mutant during the growth in human serum with 0.15 µg/mL levofloxacin
Project description:Among in silico predicted or experimentally confirmed miR-15a targets are many genes of relevance to AAA pathology and known to be down-regulated in AAA conditions. To better understand which of these targets could be linked to the observed detrimental effects of miR-15a on SMC dynamics in vitro, we performed RNA-sequencing of hAoSMCs transfected with miR-15a-modulators (mimic, inhibitor, and scrambled control). Upon transfection with miR-15a-mimic, 1030 genes were significantly down-regulated and 741 were significantly up-regulated, whereas miR-15a-inhibition led to 23 down-regulated and 82 up-regulated genes.
Project description:We intended to investigate effects of mmu-miR-15a-3p on gene expression in mice We used microarrays to compare gene expression in mouse B/CMBA.Ov cell lines transfected with mmu-miR-15a-3p and negative control mimic
Project description:MicroRNAs are important regulators of gene expression and associated with stress-related psychiatric disorders. We report that exposing mice to chronic stress led to a specific increase in microRNA-15a levels in the amygdala-Ago2 complex, and a concomitant reduction in the levels of its predicted target, FKBP51, which is implicated in stress-related psychiatric disorders. Reciprocally, mice expressing reduced levels of amygdalar microRNA-15a following exposure to chronic stress exhibited increased anxiety-like behaviors. Here, we performed small RNA Sequencing of mouse basolateral amygdala after miR15a knockdown using injection of a miR-15a sponge virus or control sponge virus.
Project description:While microRNAs (miRs) have been extensively studied in the context of malignancy and tumor progression, their functions in regulating T cell activation are less clear. We found reduced levels of miR-15a/16 at 3-18 h post-T cell receptor (TCR) stimulation, suggesting a role in shaping T cell activation. An inducible miR15a/16 transgenic mouse model was developed to determine how elevating miR-15a/16 levels during early stages of activation would affect T cell proliferation and to identify TCR signaling pathways regulated by this miR pair. Doxycyclin (DOX) induced expression of miR-15a/16 from 0-18 h post-TCR stimulation decreased ex vivo proliferation as well as in vivo antigen-specific proliferation. Bioinformatic and proteomic approaches were combined to identify MEK1 as a target of miR-15a/16. MEK1 targeting by miR-15a/16 was confirmed using miR mimics that decreased MEK1 containing the 3’-UTR target nucleotide sequence (UGCUGCUA) but did not decrease MEK1 containing a mutated control sequence (AAAAAAAA). Phosphorylation of downstream signaling molecules ERK1/2 and Elk1 were decreased with DOX-induced miR-15a/16 expression. In addition to MEK1, ERK1 was subsequently found to be targeted by miR-15a/16, with DOX induced miR-15a/16 reducing total ERK1 levels in T cells. These findings show that TCR stimulation reduces miR-15a/16 levels at early stages of T cell activation to facilitate increased MEK1 and ERK1, and this promotes sustained MEK1-ERK1/2-Elk1 signaling required for optimal proliferation.