Project description:Purpose: to profile transcriptome changes due to EC-AGO1-deficiency Methods: Subcutaneous adipose tissue were harvested. RNA was extracted using TRIzol and library was prepared for sequencing. Results: We found genes involved in pathways promoting angiogenesis, browning, insulin sensitivity to be upregulated, and those promoting inflammation and fibrosis to be decreased in KO compared with WT mice. Conclusions:Our study represents the detailed analysis of Ago1 regulate transcriptomes in SAT between WT and KO mice. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
Project description:Purpose:to reveal the changes in small RNA, esp. microRNA to correlate with transcriptome changes occuring due to EC-AGO1-KO and further explain the observed phenotype. Methods: Subcutaneous adipose tissue were harvested.Small RNA library was prepared and for sequencing. Results: We found substantial changes in miRNA due to EC-AGO1-KO. Conclusions: Our study represents the detailed analysis of Ago1 regulated small RNA transcriptomes in subcutaneous adipose tissue between WT and KO mice. We conclude that small RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
Project description:small RNA Seq of Subcutaneous adipose tissue from endothelial-AGO1-knockout (EC-AGO1-KO) mice and wild-type (WT) littermates fed 16 week of high fat high sucrose diet
Project description:Microarray expression profiles of wild-type, ago1-10, ago1-11, and dcl1-9 Arabidopsis thaliana ec. Landsberg erecta seedling at 9, 21, and 35 days after germination. Experiment Overall Design: Reference design, wild-type vs mutants, multiple biological replicates
Project description:Gene expression profiling of HUVEC (human umbilical vein EC cell; Lonza), HAEC (human aortic EC cells), HCAEC (human coronary artery EC cells), HPAEC (human pulmonary artery EC cells), HMVEC (human microvascular (dermal) , HASMC ( Human Aortic Smooth Muscle Cells), T cells and Bcells. Gene expression profiling of Endothelial cells and Non-endothelial cells in order to identify the genes with preferntial expression to endothelial cells. The experiments are performed in duplicate on both the HT Human Genome U133A and U133B arrays.
Project description:Adrenomedullin (AM) is a vasodilating peptide involved in the regulation of circulatory homeostasis and in the pathophysiology of certain cardiovascular diseases. AM plays critical roles in blood vessels, including regulation of vascular stability and permeability. To elucidate the autocrine / paracrine function of AM in endothelial cells in vivo. A conditional knockout of AM in endothelial cells (AM EC-KO) was used. The amount of vascularization the matrigel implants was lower in AM EC-KO mice indicating a defective angiogenesis. Moreover, ablation of AM in endothelial cells revealed increased vascular permeability in comparison with wildtype littermates. In addition, AM EC-KO lungs exhibited significantly less tumor growth than littermate WT mice using a syngeneic model of metastasis. Furthermore, following middle cerebral artery permanent occlusion, there was a significant infarct size decrease in animals lacking endothelial AM when compared to their wild type counterparts. AM is an important regulator of EC function, angiogenesis, tumorigenesis and brain response to ischemia. Studies of AM should bring novel approaches to the treatment of vascular diseases. Lung endothelial mRNA profiles of wild type (WT) and adrenomedullin endothelial cell conditional knockout (AM EC-KO) mice were generated by deep sequencing using Illumina GAIIx.