Project description:Single cell RNA sequencing of liver cells enriched for Non-Parenchymal cells (NPCs) to see the percentage of humanizaton, the gene signature and the heterogeneity of most types of human NPCs in a humanized liver.
Project description:To make the human liver accessible to metabolic treatments, we employed a liver-specific humanized mouse model in which approximately 50% of the mouse hepatocytes were replaced by human ones. To capture transcriptomes reflecting pathophysiology and therapeutic development of metabolic diseases, we subjected the humanized mice to dietary intervention and the key metabolic transcriptional factor agonist treatments. We then performed rna exoression profiling analysis using data obtained from nanopore direct RNA sequencing of these humanized mice.
Project description:RNAseq analysis that will help to define 1) the circadian dysfunction induced liver transcriptome that drives fatty liver disease induced hepatocarcinogenesis in a humanized mouse model; 2) the currently unknown circadian profile of NASH and HCC gene signatures specifically associated with human hepatocytes and liver or tumor microenvironment. These gene signatures will significantly advance our understanding of the mechanism of spontaneous HCC and have important preclinic values for developing novel therapeutic strategies for prevention and treatment of HCC in humans.
Project description:The goal of this experiment was to see the percentage of human reads over total (mouse and human reads) for unique hepatocyte genes that are zonated as well as for other unique genes for endothelial cells, stellate cells and cholangiocytes.
Project description:Ginkgetin could significantly attenuate liver fibrosis in a mouse model induced by TAA, including inhibiting hepatic inflammtion and fibrosis. In addition, the related signaling pathways and gene expression were also downregulated by ginkgetin by bulk RNA Sequencing analysis.
Project description:To make the human liver accessible to metabolic treatments, we employed a liver-specific humanized mouse model in which approximately 50% of the mouse hepatocytes were replaced by human ones. To capture transcriptomes reflecting pathophysiology and therapeutic development of metabolic diseases, we subjected the humanized mice to the key metabolic transcriptional factor agonist treatments. We then performed gene expression profiling analysis using data obtained from RNA-seq of these humanized mice.